The Gut Microbiome in Diabetes and Obesity: Mechanisms and Therapeutic Implications (www.kiu.ac.ug)
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About This Presentation
Diabetes and obesity, two interrelated global health epidemics, are complex metabolic disorders influenced by
genetic, environmental, and lifestyle factors. Recent evidence has illuminated the crucial role of the gut
microbiome, a vast ecosystem of microorganisms inhabiting the gastrointestinal tr...
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https://www.eejournals.org Open Access
This is an Open Access article distributed under the terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the
original work is properly cited
Page | 44
The Gut Microbiome in Diabetes and Obesity:
Mechanisms and Therapeutic Implications
Bwanbale Geoffrey David
Faculty of Pharmacy Kampala International University Uganda
ABSTRACT
Diabetes and obesity, two interrelated global health epidemics, are complex metabolic disorders influenced by
genetic, environmental, and lifestyle factors. Recent evidence has illuminated the crucial role of the gut
microbiome, a vast ecosystem of microorganisms inhabiting the gastrointestinal tract in the pathogenesis of
these conditions. Dysbiosis, or imbalance in gut microbial composition, has been consistently linked to insulin
resistance, low-grade chronic inflammation, impaired glucose metabolism, and altered energy homeostasis. This
review explores the intricate mechanisms by which the gut microbiota influences the development and
progression of diabetes and obesity, including modulation of gut barrier integrity, lipopolysaccharide-induced
inflammation, short-chain fatty acid production, bile acid signaling, and interaction with the host immune
system. We also highlight emerging therapeutic strategies targeting the gut microbiota, such as prebiotics,
probiotics, synbiotics, fecal microbiota transplantation (FMT), and microbiome-modulating drugs.
Understanding these microbial mechanisms opens new frontiers in personalized medicine for managing
metabolic disorders. This review consolidates current knowledge and identifies future directions to harness the
therapeutic potential of the gut microbiome in diabetes and obesity.
Keywords: Gut microbiome, diabetes, obesity, dysbiosis, insulin resistance, short-chain fatty acids
INTRODUCTION
Diabetes mellitus and obesity are among the most pressing global public health challenges of the 21st century,
with prevalence rates continuing to rise at an alarming pace, especially in industrialized and rapidly urbanizing
societies.[1–3] The World Health Organization (WHO) estimates that more than 500 million people are
currently living with diabetes, and over 1.9 billion adults are classified as overweight or obese globally[4–6].
These metabolic disorders are associated with a host of comorbidities, including cardiovascular disease, renal
dysfunction, neuropathy, and reduced life expectancy, making them leading contributors to the global burden
of disease.
Traditionally, the etiology of diabetes and obesity has been attributed to a combination of genetic predisposition,
poor dietary habits, sedentary lifestyles, and environmental exposures[7, 8]. However, growing scientific
interest in recent years has turned to the gut microbiome as a pivotal player in the development and progression
of metabolic diseases[9]. This interest has been spurred by advances in next-generation sequencing
technologies and metagenomic analyses, which have provided unprecedented insight into the diversity,
composition, and function of the gut microbial ecosystem[9]. The gut microbiome refers to the trillions of
microorganisms residing in the gastrointestinal tract, including bacteria, archaea, viruses, fungi, and protozoa.
These microorganisms engage in complex symbiotic interactions with the host, contributing to essential
physiological processes such as digestion, nutrient absorption, bile acid metabolism, immune modulation, and
the synthesis of vitamins and short-chain fatty acids (SCFAs)[10]. The composition of the gut microbiome is
dynamic and influenced by multiple factors, including mode of birth delivery, diet, age, antibiotic use, and
geographic location[10].
Emerging evidence suggests that disturbances in the gut microbiome collectively termed dysbiosis may have
profound implications for metabolic health[11, 12]. Dysbiosis is characterized by a loss of microbial diversity,
an overrepresentation of pathogenic bacteria, and a decline in beneficial commensals. Such imbalances have been
linked to the pathogenesis of type 2 diabetes (T2D), type 1 diabetes (T1D), and obesity through a variety of
mechanisms[13, 14]. These include increased intestinal permeability ("leaky gut"), systemic inflammation,
altered energy harvest from the diet, insulin resistance, and disruption of signaling pathways involved in glucose
and lipid metabolism[14].
EURASIAN EXPERIMENT JOURNAL OF MEDICINE AND MEDICAL SCIENCES (EEJMMS)
ISSN: 2992-4103
©EEJMMS Publications Volume 6 Issue 3 2025
This is an Open Access article distributed under the terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the
original work is properly cited
Page | 44
The Gut Microbiome in Diabetes and Obesity:
Mechanisms and Therapeutic Implications
Bwanbale Geoffrey David
Faculty of Pharmacy Kampala International University Uganda
ABSTRACT
Diabetes and obesity, two interrelated global health epidemics, are complex metabolic disorders influenced by
genetic, environmental, and lifestyle factors. Recent evidence has illuminated the crucial role of the gut
microbiome, a vast ecosystem of microorganisms inhabiting the gastrointestinal tract in the pathogenesis of
these conditions. Dysbiosis, or imbalance in gut microbial composition, has been consistently linked to insulin
resistance, low-grade chronic inflammation, impaired glucose metabolism, and altered energy homeostasis. This
review explores the intricate mechanisms by which the gut microbiota influences the development and
progression of diabetes and obesity, including modulation of gut barrier integrity, lipopolysaccharide-induced
inflammation, short-chain fatty acid production, bile acid signaling, and interaction with the host immune
system. We also highlight emerging therapeutic strategies targeting the gut microbiota, such as prebiotics,
probiotics, synbiotics, fecal microbiota transplantation (FMT), and microbiome-modulating drugs.
Understanding these microbial mechanisms opens new frontiers in personalized medicine for managing
metabolic disorders. This review consolidates current knowledge and identifies future directions to harness the
therapeutic potential of the gut microbiome in diabetes and obesity.
Keywords: Gut microbiome, diabetes, obesity, dysbiosis, insulin resistance, short-chain fatty acids
INTRODUCTION
Diabetes mellitus and obesity are among the most pressing global public health challenges of the 21st century,
with prevalence rates continuing to rise at an alarming pace, especially in industrialized and rapidly urbanizing
societies.[1–3] The World Health Organization (WHO) estimates that more than 500 million people are
currently living with diabetes, and over 1.9 billion adults are classified as overweight or obese globally[4–6].
These metabolic disorders are associated with a host of comorbidities, including cardiovascular disease, renal
dysfunction, neuropathy, and reduced life expectancy, making them leading contributors to the global burden
of disease.
Traditionally, the etiology of diabetes and obesity has been attributed to a combination of genetic predisposition,
poor dietary habits, sedentary lifestyles, and environmental exposures[7, 8]. However, growing scientific
interest in recent years has turned to the gut microbiome as a pivotal player in the development and progression
of metabolic diseases[9]. This interest has been spurred by advances in next-generation sequencing
technologies and metagenomic analyses, which have provided unprecedented insight into the diversity,
composition, and function of the gut microbial ecosystem[9]. The gut microbiome refers to the trillions of
microorganisms residing in the gastrointestinal tract, including bacteria, archaea, viruses, fungi, and protozoa.
These microorganisms engage in complex symbiotic interactions with the host, contributing to essential
physiological processes such as digestion, nutrient absorption, bile acid metabolism, immune modulation, and
the synthesis of vitamins and short-chain fatty acids (SCFAs)[10]. The composition of the gut microbiome is
dynamic and influenced by multiple factors, including mode of birth delivery, diet, age, antibiotic use, and
geographic location[10].
Emerging evidence suggests that disturbances in the gut microbiome collectively termed dysbiosis may have
profound implications for metabolic health[11, 12]. Dysbiosis is characterized by a loss of microbial diversity,
an overrepresentation of pathogenic bacteria, and a decline in beneficial commensals. Such imbalances have been
linked to the pathogenesis of type 2 diabetes (T2D), type 1 diabetes (T1D), and obesity through a variety of
mechanisms[13, 14]. These include increased intestinal permeability ("leaky gut"), systemic inflammation,
altered energy harvest from the diet, insulin resistance, and disruption of signaling pathways involved in glucose
and lipid metabolism[14].
EURASIAN EXPERIMENT JOURNAL OF MEDICINE AND MEDICAL SCIENCES (EEJMMS)
ISSN: 2992-4103
©EEJMMS Publications Volume 6 Issue 3 2025
https://www.eejournals.org Open Access
This is an Open Access article distributed under the terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the
original work is properly cited
Page | 45
In type 2 diabetes, for instance, gut microbial profiles are often marked by a reduction in butyrate-producing
bacteria such as Faecalibacterium prausnitzii, which play a role in maintaining gut barrier integrity and reducing
inflammation. Simultaneously, an enrichment of opportunistic pathogens may promote endotoxemia and
metabolic endotoxemia, exacerbating insulin resistance[15]. In type 1 diabetes, an autoimmune condition, gut
dysbiosis may contribute to the breakdown of immune tolerance and the initiation of autoimmunity against
pancreatic β-cells. Obesity, too, has been associated with distinct alterations in microbial composition, such as
an increased Firmicutes-to-Bacteroidetes ratio, which is thought to enhance energy extraction from the diet and
promote fat deposition[15]. Given the intricate and bidirectional relationship between the gut microbiome and
host metabolic health, there is growing interest in microbiome-targeted interventions as potential therapeutic
strategies for diabetes and obesity. These strategies include the use of prebiotics, probiotics, synbiotics, fecal
microbiota transplantation (FMT), and dietary modifications aimed at restoring a balanced microbial
community. Understanding the underlying mechanisms by which the gut microbiota influences metabolic
homeostasis is crucial for developing effective, personalized treatments for these chronic diseases[15]. This
review aims to explore the current knowledge on the role of the gut microbiome in the development and
management of diabetes and obesity, elucidating the underlying mechanisms and highlighting therapeutic
implications. By understanding the complex interplay between host and microbiota, we can move closer to
microbiome-based precision medicine in metabolic disease management.
Composition and Functions of the Gut Microbiome
The adult human gastrointestinal tract is home to an extraordinarily complex and dense microbial ecosystem,
often referred to as the gut microbiota. This dynamic community consists of trillions of microorganisms,
including bacteria, archaea, viruses, and fungi. Among the bacterial inhabitants, the phyla Firmicutes and
Bacteroidetes dominate, comprising more than 90% of the gut microbial population. These microbial residents
are not passive bystanders; rather, they play crucial roles in maintaining host health through a wide range of
biochemical, immunological, and metabolic activities that contribute to the overall physiological homeostasis of
the human body[16].
One of the most well-documented functions of the gut microbiota is the fermentation of indigestible dietary
fibers, a complex carbohydrate that escape digestion in the upper gastrointestinal tract. Once these fibers reach
the colon, they serve as substrates for microbial fermentation, leading to the production of short-chain fatty
acids (SCFAs) such as butyrate, propionate, and acetate[17]. Each of these SCFAs exerts unique physiological
effects. Butyrate, for example, serves as a primary energy source for colonocytes, promotes the integrity of the
intestinal lining, and possesses anti-inflammatory properties. Propionate is absorbed into the bloodstream and
transported to the liver, where it influences gluconeogenesis and satiety signaling[18]. Acetate, the most
abundant SCFA, enters systemic circulation and is utilized in peripheral tissues, including muscle and adipose
tissue, thereby participating in cholesterol metabolism and appetite regulation. Together, these metabolites not
only provide energy but also modulate host metabolism, influence lipid and glucose homeostasis, and contribute
to the prevention of metabolic disorders such as obesity and type 2 diabetes[18].
Beyond metabolic contributions, the gut microbiota plays an indispensable role in the regulation of the host
immune system. From early life through adulthood, microbial exposure is essential for the maturation of both
innate and adaptive immunity. The gut microbiota engages in a continuous crosstalk with the host's immune
cells, facilitating immune tolerance to harmless antigens while enhancing the ability to mount effective responses
against pathogenic organisms[19]. This immunomodulatory function involves complex signaling pathways,
including the stimulation of pattern recognition receptors such as Toll-like receptors (TLRs) and the production
of microbial metabolites that affect the activity of regulatory T cells (Tregs) and dendritic cells. SCFAs,
particularly butyrate, enhance the differentiation of Tregs, which are essential for maintaining immune tolerance
and suppressing inflammatory responses. Consequently, disruptions in the microbial composition, a condition
known as dysbiosis, are often linked to the development of autoimmune and inflammatory diseases, including
inflammatory bowel disease (IBD), allergies, and even neuroinflammatory conditions[19].
Another critical function of the gut microbiota is its role in maintaining the integrity of the intestinal barrier.
The gut epithelium acts as a selective barrier that allows nutrient absorption while preventing the translocation
of pathogens, toxins, and antigens into the systemic circulation[20]. Commensal microbes support this barrier
through several mechanisms, including the stimulation of mucin production, strengthening of tight junction
proteins, and inhibition of pathogenic bacterial colonization. For example, butyrate has been shown to
upregulate the expression of tight junction proteins such as claudins and occludins, reinforcing epithelial
integrity and reducing intestinal permeability often referred to as “leaky gut.” When this barrier function is
compromised, it can lead to systemic inflammation and has been implicated in a variety of chronic diseases,
including metabolic syndrome, cardiovascular disease, and neurological disorders[21].
In addition to fermentation and immune regulation, the gut microbiota is heavily involved in bile acid
metabolism, a process that significantly influences lipid and glucose homeostasis. Primary bile acids are
synthesized in the liver from cholesterol and secreted into the intestine, where they aid in the digestion and
absorption of dietary fats[22]. Gut microbes subsequently convert these primary bile acids into secondary bile
This is an Open Access article distributed under the terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the
original work is properly cited
Page | 45
In type 2 diabetes, for instance, gut microbial profiles are often marked by a reduction in butyrate-producing
bacteria such as Faecalibacterium prausnitzii, which play a role in maintaining gut barrier integrity and reducing
inflammation. Simultaneously, an enrichment of opportunistic pathogens may promote endotoxemia and
metabolic endotoxemia, exacerbating insulin resistance[15]. In type 1 diabetes, an autoimmune condition, gut
dysbiosis may contribute to the breakdown of immune tolerance and the initiation of autoimmunity against
pancreatic β-cells. Obesity, too, has been associated with distinct alterations in microbial composition, such as
an increased Firmicutes-to-Bacteroidetes ratio, which is thought to enhance energy extraction from the diet and
promote fat deposition[15]. Given the intricate and bidirectional relationship between the gut microbiome and
host metabolic health, there is growing interest in microbiome-targeted interventions as potential therapeutic
strategies for diabetes and obesity. These strategies include the use of prebiotics, probiotics, synbiotics, fecal
microbiota transplantation (FMT), and dietary modifications aimed at restoring a balanced microbial
community. Understanding the underlying mechanisms by which the gut microbiota influences metabolic
homeostasis is crucial for developing effective, personalized treatments for these chronic diseases[15]. This
review aims to explore the current knowledge on the role of the gut microbiome in the development and
management of diabetes and obesity, elucidating the underlying mechanisms and highlighting therapeutic
implications. By understanding the complex interplay between host and microbiota, we can move closer to
microbiome-based precision medicine in metabolic disease management.
Composition and Functions of the Gut Microbiome
The adult human gastrointestinal tract is home to an extraordinarily complex and dense microbial ecosystem,
often referred to as the gut microbiota. This dynamic community consists of trillions of microorganisms,
including bacteria, archaea, viruses, and fungi. Among the bacterial inhabitants, the phyla Firmicutes and
Bacteroidetes dominate, comprising more than 90% of the gut microbial population. These microbial residents
are not passive bystanders; rather, they play crucial roles in maintaining host health through a wide range of
biochemical, immunological, and metabolic activities that contribute to the overall physiological homeostasis of
the human body[16].
One of the most well-documented functions of the gut microbiota is the fermentation of indigestible dietary
fibers, a complex carbohydrate that escape digestion in the upper gastrointestinal tract. Once these fibers reach
the colon, they serve as substrates for microbial fermentation, leading to the production of short-chain fatty
acids (SCFAs) such as butyrate, propionate, and acetate[17]. Each of these SCFAs exerts unique physiological
effects. Butyrate, for example, serves as a primary energy source for colonocytes, promotes the integrity of the
intestinal lining, and possesses anti-inflammatory properties. Propionate is absorbed into the bloodstream and
transported to the liver, where it influences gluconeogenesis and satiety signaling[18]. Acetate, the most
abundant SCFA, enters systemic circulation and is utilized in peripheral tissues, including muscle and adipose
tissue, thereby participating in cholesterol metabolism and appetite regulation. Together, these metabolites not
only provide energy but also modulate host metabolism, influence lipid and glucose homeostasis, and contribute
to the prevention of metabolic disorders such as obesity and type 2 diabetes[18].
Beyond metabolic contributions, the gut microbiota plays an indispensable role in the regulation of the host
immune system. From early life through adulthood, microbial exposure is essential for the maturation of both
innate and adaptive immunity. The gut microbiota engages in a continuous crosstalk with the host's immune
cells, facilitating immune tolerance to harmless antigens while enhancing the ability to mount effective responses
against pathogenic organisms[19]. This immunomodulatory function involves complex signaling pathways,
including the stimulation of pattern recognition receptors such as Toll-like receptors (TLRs) and the production
of microbial metabolites that affect the activity of regulatory T cells (Tregs) and dendritic cells. SCFAs,
particularly butyrate, enhance the differentiation of Tregs, which are essential for maintaining immune tolerance
and suppressing inflammatory responses. Consequently, disruptions in the microbial composition, a condition
known as dysbiosis, are often linked to the development of autoimmune and inflammatory diseases, including
inflammatory bowel disease (IBD), allergies, and even neuroinflammatory conditions[19].
Another critical function of the gut microbiota is its role in maintaining the integrity of the intestinal barrier.
The gut epithelium acts as a selective barrier that allows nutrient absorption while preventing the translocation
of pathogens, toxins, and antigens into the systemic circulation[20]. Commensal microbes support this barrier
through several mechanisms, including the stimulation of mucin production, strengthening of tight junction
proteins, and inhibition of pathogenic bacterial colonization. For example, butyrate has been shown to
upregulate the expression of tight junction proteins such as claudins and occludins, reinforcing epithelial
integrity and reducing intestinal permeability often referred to as “leaky gut.” When this barrier function is
compromised, it can lead to systemic inflammation and has been implicated in a variety of chronic diseases,
including metabolic syndrome, cardiovascular disease, and neurological disorders[21].
In addition to fermentation and immune regulation, the gut microbiota is heavily involved in bile acid
metabolism, a process that significantly influences lipid and glucose homeostasis. Primary bile acids are
synthesized in the liver from cholesterol and secreted into the intestine, where they aid in the digestion and
absorption of dietary fats[22]. Gut microbes subsequently convert these primary bile acids into secondary bile
https://www.eejournals.org Open Access
This is an Open Access article distributed under the terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the
original work is properly cited
Page | 46
acids through enzymatic deconjugation and dehydroxylation processes. These secondary bile acids function as
signaling molecules that interact with host receptors such as the farnesoid X receptor (FXR) and the G protein-
coupled bile acid receptor (TGR5). Activation of these receptors influences various metabolic pathways,
including those involved in lipid synthesis, glucose metabolism, and energy expenditure[23]. Thus, the
microbiota-mediated modification of bile acids represents a key mechanism by which gut microbes can exert
systemic effects on host metabolism and contribute to the development or prevention of metabolic
disorders[23].
In sum, the gut microbiota performs an array of vital functions that are essential for human health. Through the
fermentation of dietary fibers into SCFAs, modulation of immune responses, reinforcement of the gut barrier,
and regulation of bile acid metabolism, this microbial community plays a central role in metabolic, immune, and
gastrointestinal homeostasis. An imbalance in this finely tuned ecosystem can have profound implications,
underscoring the importance of maintaining a healthy gut microbiome through diet, lifestyle, and, when
necessary, therapeutic interventions.
Gut Microbiome and Obesity
Microbiota Composition in Obesity
The composition of the gut microbiota plays a significant role in the development and progression of obesity.
Numerous studies have consistently shown that obese individuals tend to have a distinctive microbial signature
when compared to lean individuals. One of the most notable observations is an increased Firmicutes-to-
Bacteroidetes ratio. This shift is thought to favor the extraction of energy from the diet, thereby contributing
to excessive caloric availability[24]. In addition, obesity is often associated with a reduction in overall microbial
diversity, a hallmark of dysbiosis. A diverse gut microbiome is generally considered beneficial, as it reflects a
more resilient and functionally stable microbial community. Reduced diversity in obese individuals suggests a
loss of important microbial functions and ecological niches, potentially leading to imbalances that promote
metabolic dysfunction[24].
Moreover, specific microbial taxa known to confer metabolic benefits are often depleted in obesity. For example,
Akkermansia muciniphila, a mucin-degrading bacterium associated with improved gut barrier function and anti-
inflammatory effects, is typically found in lower abundance in obese individuals[25]. The depletion of
Akkermansia may contribute to increased gut permeability and systemic inflammation, two processes commonly
linked to obesity-related metabolic disorders. Similarly, levels of Bifidobacterium species, known for their
probiotic effects and ability to modulate immune responses, are also reduced in obesity. These bacteria help
maintain intestinal integrity and produce metabolites that influence host metabolism favorably. Their decreased
presence further underscores the compromised metabolic environment in obese individuals[25].
The changes in microbiota composition observed in obesity are influenced by a range of factors, including diet,
genetics, lifestyle, and environmental exposures. Diet, particularly the consumption of high-fat and low-fiber
foods, is a major modulator of microbial structure. Such dietary patterns promote the growth of bacteria that
may encourage energy storage, low-grade inflammation, and insulin resistance[25]. Furthermore, the gut
microbiota in obesity is often less responsive to dietary interventions, potentially hindering weight loss
efforts[26]. Understanding the complex relationships between microbiota composition and obesity may provide
new insights into therapeutic strategies. Interventions such as prebiotics, probiotics, dietary modification, and
even fecal microbiota transplantation are being explored as ways to restore a healthy gut microbial balance and
combat obesity-related metabolic impairments.
Mechanistic Insights
The gut microbiota contributes to obesity through several interrelated mechanisms that involve energy
regulation, metabolic signaling, and inflammation[27]. One of the key pathways is enhanced energy harvesting
from the diet. Gut microbes possess a diverse array of enzymes capable of breaking down complex
polysaccharides that are otherwise indigestible by human enzymes[27]. These polysaccharides are fermented
into short-chain fatty acids (SCFAs) such as acetate, propionate, and butyrate, which serve as additional energy
sources. The increased production and absorption of these microbial metabolites provide more calories to the
host, potentially leading to a positive energy balance and weight gain over time. This enhanced energy
extraction is particularly pronounced in microbiota dominated by Firmicutes, which are efficient fermenters.
While SCFAs generally have beneficial roles in regulating gut health, inflammation, and satiety, excessive SCFA
production in the context of obesity may contribute to metabolic disturbances. Specifically, acetate and butyrate
have been shown to stimulate lipogenesis in the liver, increasing fat deposition. Moreover, acetate may act as a
substrate for cholesterol and fatty acid synthesis, further promoting adiposity. Thus, although SCFAs are
essential for maintaining colonic health and energy homeostasis, their overproduction in an obese microbiome
can paradoxically facilitate fat accumulation[28].
Another critical mechanism is the development of metabolic endotoxemia, which is largely influenced by dietary
patterns. High-fat diets can disrupt gut barrier function by altering the expression of tight junction proteins,
increasing intestinal permeability. This compromised barrier allows bacterial components such as
lipopolysaccharides (LPS) from gram-negative bacteria to translocate into the systemic circulation. Circulating
This is an Open Access article distributed under the terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the
original work is properly cited
Page | 46
acids through enzymatic deconjugation and dehydroxylation processes. These secondary bile acids function as
signaling molecules that interact with host receptors such as the farnesoid X receptor (FXR) and the G protein-
coupled bile acid receptor (TGR5). Activation of these receptors influences various metabolic pathways,
including those involved in lipid synthesis, glucose metabolism, and energy expenditure[23]. Thus, the
microbiota-mediated modification of bile acids represents a key mechanism by which gut microbes can exert
systemic effects on host metabolism and contribute to the development or prevention of metabolic
disorders[23].
In sum, the gut microbiota performs an array of vital functions that are essential for human health. Through the
fermentation of dietary fibers into SCFAs, modulation of immune responses, reinforcement of the gut barrier,
and regulation of bile acid metabolism, this microbial community plays a central role in metabolic, immune, and
gastrointestinal homeostasis. An imbalance in this finely tuned ecosystem can have profound implications,
underscoring the importance of maintaining a healthy gut microbiome through diet, lifestyle, and, when
necessary, therapeutic interventions.
Gut Microbiome and Obesity
Microbiota Composition in Obesity
The composition of the gut microbiota plays a significant role in the development and progression of obesity.
Numerous studies have consistently shown that obese individuals tend to have a distinctive microbial signature
when compared to lean individuals. One of the most notable observations is an increased Firmicutes-to-
Bacteroidetes ratio. This shift is thought to favor the extraction of energy from the diet, thereby contributing
to excessive caloric availability[24]. In addition, obesity is often associated with a reduction in overall microbial
diversity, a hallmark of dysbiosis. A diverse gut microbiome is generally considered beneficial, as it reflects a
more resilient and functionally stable microbial community. Reduced diversity in obese individuals suggests a
loss of important microbial functions and ecological niches, potentially leading to imbalances that promote
metabolic dysfunction[24].
Moreover, specific microbial taxa known to confer metabolic benefits are often depleted in obesity. For example,
Akkermansia muciniphila, a mucin-degrading bacterium associated with improved gut barrier function and anti-
inflammatory effects, is typically found in lower abundance in obese individuals[25]. The depletion of
Akkermansia may contribute to increased gut permeability and systemic inflammation, two processes commonly
linked to obesity-related metabolic disorders. Similarly, levels of Bifidobacterium species, known for their
probiotic effects and ability to modulate immune responses, are also reduced in obesity. These bacteria help
maintain intestinal integrity and produce metabolites that influence host metabolism favorably. Their decreased
presence further underscores the compromised metabolic environment in obese individuals[25].
The changes in microbiota composition observed in obesity are influenced by a range of factors, including diet,
genetics, lifestyle, and environmental exposures. Diet, particularly the consumption of high-fat and low-fiber
foods, is a major modulator of microbial structure. Such dietary patterns promote the growth of bacteria that
may encourage energy storage, low-grade inflammation, and insulin resistance[25]. Furthermore, the gut
microbiota in obesity is often less responsive to dietary interventions, potentially hindering weight loss
efforts[26]. Understanding the complex relationships between microbiota composition and obesity may provide
new insights into therapeutic strategies. Interventions such as prebiotics, probiotics, dietary modification, and
even fecal microbiota transplantation are being explored as ways to restore a healthy gut microbial balance and
combat obesity-related metabolic impairments.
Mechanistic Insights
The gut microbiota contributes to obesity through several interrelated mechanisms that involve energy
regulation, metabolic signaling, and inflammation[27]. One of the key pathways is enhanced energy harvesting
from the diet. Gut microbes possess a diverse array of enzymes capable of breaking down complex
polysaccharides that are otherwise indigestible by human enzymes[27]. These polysaccharides are fermented
into short-chain fatty acids (SCFAs) such as acetate, propionate, and butyrate, which serve as additional energy
sources. The increased production and absorption of these microbial metabolites provide more calories to the
host, potentially leading to a positive energy balance and weight gain over time. This enhanced energy
extraction is particularly pronounced in microbiota dominated by Firmicutes, which are efficient fermenters.
While SCFAs generally have beneficial roles in regulating gut health, inflammation, and satiety, excessive SCFA
production in the context of obesity may contribute to metabolic disturbances. Specifically, acetate and butyrate
have been shown to stimulate lipogenesis in the liver, increasing fat deposition. Moreover, acetate may act as a
substrate for cholesterol and fatty acid synthesis, further promoting adiposity. Thus, although SCFAs are
essential for maintaining colonic health and energy homeostasis, their overproduction in an obese microbiome
can paradoxically facilitate fat accumulation[28].
Another critical mechanism is the development of metabolic endotoxemia, which is largely influenced by dietary
patterns. High-fat diets can disrupt gut barrier function by altering the expression of tight junction proteins,
increasing intestinal permeability. This compromised barrier allows bacterial components such as
lipopolysaccharides (LPS) from gram-negative bacteria to translocate into the systemic circulation. Circulating
https://www.eejournals.org Open Access
This is an Open Access article distributed under the terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the
original work is properly cited
Page | 47
LPS is recognized by the immune system as a danger signal and can trigger low-grade, chronic inflammation
through the activation of Toll-like receptor 4 (TLR4)[29]. This inflammatory state is a major driver of insulin
resistance and other metabolic derangements seen in obesity.
These microbiota-mediated mechanisms underscore the dynamic interplay between the gut and host
metabolism. They illustrate how microbial activities extend beyond digestion and profoundly influence energy
storage, immune responses, and systemic metabolic outcomes. Unraveling these mechanisms not only deepens
our understanding of obesity pathophysiology but also opens new avenues for therapeutic targeting of the gut
microbiome. Strategies such as dietary modulation, selective microbiota enrichment, and anti-inflammatory
interventions hold promise in mitigating the impact of gut-derived signals on obesity and its associated
complications.
Gut Microbiome and Diabetes
Type 2 Diabetes (T2D)
Type 2 diabetes (T2D) is a complex metabolic disorder primarily marked by chronic hyperglycemia, which
results from a combination of insulin resistance and progressive β-cell dysfunction[1, 30, 31]. The gut
microbiota has emerged as a significant modulator in T2D pathogenesis. Patients with T2D often exhibit a state
of gut dysbiosis, characterized by decreased microbial diversity and specific compositional shifts. One notable
alteration is the reduced abundance of Faecalibacterium prausnitzii, a prominent butyrate-producing bacterium
known for its anti-inflammatory properties and role in maintaining gut barrier integrity. At the same time, there
is often an increase in opportunistic and potentially pro-inflammatory bacterial taxa such as Ruminococcus gnavus
and Bacteroides[13, 14]. These microbial imbalances contribute to a systemic pro-inflammatory environment
and can exacerbate insulin resistance. Furthermore, altered microbial metabolism in T2D affects the production
of short-chain fatty acids (SCFAs) and branched-chain amino acids (BCAAs), both of which are critical in energy
metabolism and insulin signaling. The gut-liver axis also becomes impaired, leading to dysregulated bile acid
signaling and increased endotoxemia. Together, these changes suggest that targeting the gut microbiome may
offer a promising therapeutic avenue for T2D prevention and management[32].
Type 1 Diabetes (T1D)
Type 1 diabetes (T1D) is an autoimmune condition characterized by the destruction of pancreatic β-cells, leading
to absolute insulin deficiency. While the genetic predisposition plays a critical role in T1D, environmental
factors, especially gut microbiota alterations, are increasingly recognized as crucial in disease onset and
progression[33]. Studies have shown that children at risk for T1D often exhibit early-life microbial dysbiosis
marked by reduced bacterial diversity and a lower abundance of beneficial SCFA-producing bacteria such as
Bifidobacterium and Akkermansia. These beneficial microbes are known for their role in regulating gut barrier
function, maintaining immune homeostasis, and suppressing inflammation[34]. A compromised gut barrier due
to decreased SCFA levels can lead to increased intestinal permeability or "leaky gut," allowing microbial
antigens and endotoxins to enter circulation and trigger systemic immune responses. This heightened immune
activity may contribute to the breakdown of self-tolerance and the activation of autoreactive T cells against
pancreatic β-cells. Additionally, the timing of microbiota shifts, especially during critical windows of immune
development in early childhood, appears to influence the trajectory toward autoimmunity[35]. Understanding
these microbiota-host interactions opens up potential for microbiome-based interventions as preventive
strategies in high-risk individuals.
Key Mechanisms
Several interrelated mechanisms link gut microbiota alterations to the development and progression of diabetes.
One central mechanism is gut barrier dysfunction. In both T1D and T2D, increased intestinal permeability often
referred to as "leaky gut" permits the translocation of microbial antigens, endotoxins, and other inflammatory
stimuli into the bloodstream. This promotes systemic immune activation and low-grade inflammation, which
contributes to insulin resistance and autoimmunity. Another crucial mechanism involves immune
modulation[36]. The gut microbiota plays a key role in shaping immune responses by influencing T cell
differentiation. In the context of diabetes, altered microbial antigen presentation and SCFA deficiencies can skew
immune responses toward pro-inflammatory T helper 1 (Th1) and Th17 phenotypes, exacerbating immune-
mediated β-cell destruction in T1D and insulin resistance in T2D. Additionally, bile acid metabolism is
significantly influenced by the gut microbiota. Secondary bile acids, produced by microbial enzymes, can bind
to host receptors such as farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5)[37].
Activation of these receptors affects glucose and lipid metabolism, energy expenditure, and insulin sensitivity.
Dysbiosis disrupts this bile acid signaling axis, further impairing metabolic homeostasis. Collectively, these
mechanisms highlight the gut microbiota as a critical interface in the pathophysiology of diabetes[37].
Therapeutic Implications
Probiotics
Probiotics are live microorganisms that, when administered in adequate amounts, confer health benefits to the
host. Specific strains such as Lactobacillus and Bifidobacterium have been shown to improve metabolic health,
This is an Open Access article distributed under the terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the
original work is properly cited
Page | 47
LPS is recognized by the immune system as a danger signal and can trigger low-grade, chronic inflammation
through the activation of Toll-like receptor 4 (TLR4)[29]. This inflammatory state is a major driver of insulin
resistance and other metabolic derangements seen in obesity.
These microbiota-mediated mechanisms underscore the dynamic interplay between the gut and host
metabolism. They illustrate how microbial activities extend beyond digestion and profoundly influence energy
storage, immune responses, and systemic metabolic outcomes. Unraveling these mechanisms not only deepens
our understanding of obesity pathophysiology but also opens new avenues for therapeutic targeting of the gut
microbiome. Strategies such as dietary modulation, selective microbiota enrichment, and anti-inflammatory
interventions hold promise in mitigating the impact of gut-derived signals on obesity and its associated
complications.
Gut Microbiome and Diabetes
Type 2 Diabetes (T2D)
Type 2 diabetes (T2D) is a complex metabolic disorder primarily marked by chronic hyperglycemia, which
results from a combination of insulin resistance and progressive β-cell dysfunction[1, 30, 31]. The gut
microbiota has emerged as a significant modulator in T2D pathogenesis. Patients with T2D often exhibit a state
of gut dysbiosis, characterized by decreased microbial diversity and specific compositional shifts. One notable
alteration is the reduced abundance of Faecalibacterium prausnitzii, a prominent butyrate-producing bacterium
known for its anti-inflammatory properties and role in maintaining gut barrier integrity. At the same time, there
is often an increase in opportunistic and potentially pro-inflammatory bacterial taxa such as Ruminococcus gnavus
and Bacteroides[13, 14]. These microbial imbalances contribute to a systemic pro-inflammatory environment
and can exacerbate insulin resistance. Furthermore, altered microbial metabolism in T2D affects the production
of short-chain fatty acids (SCFAs) and branched-chain amino acids (BCAAs), both of which are critical in energy
metabolism and insulin signaling. The gut-liver axis also becomes impaired, leading to dysregulated bile acid
signaling and increased endotoxemia. Together, these changes suggest that targeting the gut microbiome may
offer a promising therapeutic avenue for T2D prevention and management[32].
Type 1 Diabetes (T1D)
Type 1 diabetes (T1D) is an autoimmune condition characterized by the destruction of pancreatic β-cells, leading
to absolute insulin deficiency. While the genetic predisposition plays a critical role in T1D, environmental
factors, especially gut microbiota alterations, are increasingly recognized as crucial in disease onset and
progression[33]. Studies have shown that children at risk for T1D often exhibit early-life microbial dysbiosis
marked by reduced bacterial diversity and a lower abundance of beneficial SCFA-producing bacteria such as
Bifidobacterium and Akkermansia. These beneficial microbes are known for their role in regulating gut barrier
function, maintaining immune homeostasis, and suppressing inflammation[34]. A compromised gut barrier due
to decreased SCFA levels can lead to increased intestinal permeability or "leaky gut," allowing microbial
antigens and endotoxins to enter circulation and trigger systemic immune responses. This heightened immune
activity may contribute to the breakdown of self-tolerance and the activation of autoreactive T cells against
pancreatic β-cells. Additionally, the timing of microbiota shifts, especially during critical windows of immune
development in early childhood, appears to influence the trajectory toward autoimmunity[35]. Understanding
these microbiota-host interactions opens up potential for microbiome-based interventions as preventive
strategies in high-risk individuals.
Key Mechanisms
Several interrelated mechanisms link gut microbiota alterations to the development and progression of diabetes.
One central mechanism is gut barrier dysfunction. In both T1D and T2D, increased intestinal permeability often
referred to as "leaky gut" permits the translocation of microbial antigens, endotoxins, and other inflammatory
stimuli into the bloodstream. This promotes systemic immune activation and low-grade inflammation, which
contributes to insulin resistance and autoimmunity. Another crucial mechanism involves immune
modulation[36]. The gut microbiota plays a key role in shaping immune responses by influencing T cell
differentiation. In the context of diabetes, altered microbial antigen presentation and SCFA deficiencies can skew
immune responses toward pro-inflammatory T helper 1 (Th1) and Th17 phenotypes, exacerbating immune-
mediated β-cell destruction in T1D and insulin resistance in T2D. Additionally, bile acid metabolism is
significantly influenced by the gut microbiota. Secondary bile acids, produced by microbial enzymes, can bind
to host receptors such as farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5)[37].
Activation of these receptors affects glucose and lipid metabolism, energy expenditure, and insulin sensitivity.
Dysbiosis disrupts this bile acid signaling axis, further impairing metabolic homeostasis. Collectively, these
mechanisms highlight the gut microbiota as a critical interface in the pathophysiology of diabetes[37].
Therapeutic Implications
Probiotics
Probiotics are live microorganisms that, when administered in adequate amounts, confer health benefits to the
host. Specific strains such as Lactobacillus and Bifidobacterium have been shown to improve metabolic health,
https://www.eejournals.org Open Access
This is an Open Access article distributed under the terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the
original work is properly cited
Page | 48
particularly in individuals with obesity and diabetes.[38] Clinical trials demonstrate that probiotic
supplementation can enhance insulin sensitivity, reduce systemic inflammation, and improve lipid profiles by
restoring gut microbial balance[39]. These effects are largely mediated through modulation of gut permeability,
reduction of pro-inflammatory cytokines, and increased production of beneficial short-chain fatty acids (SCFAs).
Continued research is uncovering strain-specific effects and optimal dosing strategies for metabolic disease
management.[39]
Prebiotics and Synbiotics
Prebiotics are non-digestible food components such as inulin, fructooligosaccharides (FOS), and
galactooligosaccharides (GOS) that selectively stimulate the growth and activity of beneficial gut bacteria. Their
fermentation by the gut microbiota leads to the production of SCFAs, which play crucial roles in energy
metabolism, inflammation control, and gut barrier integrity[40]. Synbiotics, which combine probiotics and
prebiotics, offer synergistic benefits by enhancing the survival and colonization of beneficial microbes while
simultaneously fueling their activity. Together, these compounds have been associated with improved glucose
homeostasis, lipid metabolism, and immune modulation in individuals with obesity or type 2 diabetes, making
them valuable tools for metabolic intervention[40].
Fecal Microbiota Transplantation (FMT)
Fecal Microbiota Transplantation (FMT) involves the transfer of stool containing a complex microbial
community from a healthy donor to the gastrointestinal tract of a recipient. Initially successful in treating
recurrent Clostridioides difficile infections, FMT has recently shown promise in metabolic disease contexts[41].
Early clinical studies report that FMT from lean, healthy donors to individuals with metabolic syndrome can
transiently improve insulin sensitivity and reduce markers of systemic inflammation[41]. The beneficial effects
are thought to stem from restored microbial diversity and functional shifts in metabolite production, including
SCFAs and bile acids. However, long-term efficacy and safety require further investigation.
Microbiome-Modulating Drugs
Microbiome-modulating drugs represent a new frontier in precision medicine, targeting microbial pathways
that influence host metabolism. These therapeutics are designed to selectively enhance or inhibit specific
microbial functions, such as short-chain fatty acid production, lipopolysaccharide (LPS) biosynthesis, and bile
acid transformation[42]. For example, drugs that promote SCFA synthesis may improve insulin sensitivity and
reduce inflammation, while inhibitors of LPS production could attenuate metabolic endotoxemia. Some agents
also modulate gut-brain signaling pathways involved in appetite regulation[43]. Unlike broad-spectrum
antibiotics, these drugs offer targeted intervention without disrupting overall microbial balance. They hold
great promise for treating diabetes and obesity with minimal side effects.
Diet and Lifestyle
Diet and lifestyle choices are among the most powerful modulators of the gut microbiome. Diets rich in fiber,
polyphenols, and plant-based components such as the Mediterranean diet foster microbial diversity and the
abundance of beneficial taxa like Akkermansia muciniphila and Bifidobacterium[44]. These bacteria contribute to
enhanced SCFA production, improved gut barrier integrity, and reduced systemic inflammation. Conversely,
high-fat, low-fiber Western diets promote dysbiosis and metabolic dysfunction. Physical activity also supports
a healthier microbiome by enhancing microbial richness and metabolic resilience. Sustainable dietary and
lifestyle interventions not only shift microbial composition favorably but also help in long-term management of
obesity and diabetes[44].
Future Perspectives
Although microbiome-based therapies show great promise, challenges remain, including inter-individual
variability, regulatory hurdles, and long-term safety. Integrating multi-omics approaches—metagenomics,
metabolomics, and transcriptomics—will enable more precise characterization of microbiome–host interactions.
Personalized nutrition and targeted microbial interventions represent the frontier of metabolic disease
management.
CONCLUSION
The gut microbiome is a central player in the pathogenesis and potential treatment of diabetes and obesity.
Mechanistic insights into microbial regulation of host metabolism have paved the way for innovative therapeutic
strategies. A deeper understanding of microbial ecology, host genetics, and environmental influences will be
critical to fully harness the microbiome’s therapeutic potential in combating metabolic diseases.
REFERENCES
1. Chandrasekaran, P., Weiskirchen, R.: The Role of Obesity in Type 2 Diabetes Mellitus—An Overview.
International Journal of Molecular Sciences. 25, 1882 (2024). https://doi.org/10.3390/ijms25031882
2. Chellappan, D.K., Chellian, J., Rahmah, N.S.N., Gan, W.J., Banerjee, P., Sanyal, S., Banerjee, P., Ghosh,
N., Guith, T., Das, A., Gupta, G., Singh, S.K., Dua, K., Kunnath, A.P., Norhashim, N.A., Ong, K.H.,
Palaniveloo, K.: Hypoglycaemic Molecules for the Management of Diabetes Mellitus from Marine
Sources. DMSO. 16, 2187–2223 (2023). https://doi.org/10.2147/DMSO.S390741
This is an Open Access article distributed under the terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the
original work is properly cited
Page | 48
particularly in individuals with obesity and diabetes.[38] Clinical trials demonstrate that probiotic
supplementation can enhance insulin sensitivity, reduce systemic inflammation, and improve lipid profiles by
restoring gut microbial balance[39]. These effects are largely mediated through modulation of gut permeability,
reduction of pro-inflammatory cytokines, and increased production of beneficial short-chain fatty acids (SCFAs).
Continued research is uncovering strain-specific effects and optimal dosing strategies for metabolic disease
management.[39]
Prebiotics and Synbiotics
Prebiotics are non-digestible food components such as inulin, fructooligosaccharides (FOS), and
galactooligosaccharides (GOS) that selectively stimulate the growth and activity of beneficial gut bacteria. Their
fermentation by the gut microbiota leads to the production of SCFAs, which play crucial roles in energy
metabolism, inflammation control, and gut barrier integrity[40]. Synbiotics, which combine probiotics and
prebiotics, offer synergistic benefits by enhancing the survival and colonization of beneficial microbes while
simultaneously fueling their activity. Together, these compounds have been associated with improved glucose
homeostasis, lipid metabolism, and immune modulation in individuals with obesity or type 2 diabetes, making
them valuable tools for metabolic intervention[40].
Fecal Microbiota Transplantation (FMT)
Fecal Microbiota Transplantation (FMT) involves the transfer of stool containing a complex microbial
community from a healthy donor to the gastrointestinal tract of a recipient. Initially successful in treating
recurrent Clostridioides difficile infections, FMT has recently shown promise in metabolic disease contexts[41].
Early clinical studies report that FMT from lean, healthy donors to individuals with metabolic syndrome can
transiently improve insulin sensitivity and reduce markers of systemic inflammation[41]. The beneficial effects
are thought to stem from restored microbial diversity and functional shifts in metabolite production, including
SCFAs and bile acids. However, long-term efficacy and safety require further investigation.
Microbiome-Modulating Drugs
Microbiome-modulating drugs represent a new frontier in precision medicine, targeting microbial pathways
that influence host metabolism. These therapeutics are designed to selectively enhance or inhibit specific
microbial functions, such as short-chain fatty acid production, lipopolysaccharide (LPS) biosynthesis, and bile
acid transformation[42]. For example, drugs that promote SCFA synthesis may improve insulin sensitivity and
reduce inflammation, while inhibitors of LPS production could attenuate metabolic endotoxemia. Some agents
also modulate gut-brain signaling pathways involved in appetite regulation[43]. Unlike broad-spectrum
antibiotics, these drugs offer targeted intervention without disrupting overall microbial balance. They hold
great promise for treating diabetes and obesity with minimal side effects.
Diet and Lifestyle
Diet and lifestyle choices are among the most powerful modulators of the gut microbiome. Diets rich in fiber,
polyphenols, and plant-based components such as the Mediterranean diet foster microbial diversity and the
abundance of beneficial taxa like Akkermansia muciniphila and Bifidobacterium[44]. These bacteria contribute to
enhanced SCFA production, improved gut barrier integrity, and reduced systemic inflammation. Conversely,
high-fat, low-fiber Western diets promote dysbiosis and metabolic dysfunction. Physical activity also supports
a healthier microbiome by enhancing microbial richness and metabolic resilience. Sustainable dietary and
lifestyle interventions not only shift microbial composition favorably but also help in long-term management of
obesity and diabetes[44].
Future Perspectives
Although microbiome-based therapies show great promise, challenges remain, including inter-individual
variability, regulatory hurdles, and long-term safety. Integrating multi-omics approaches—metagenomics,
metabolomics, and transcriptomics—will enable more precise characterization of microbiome–host interactions.
Personalized nutrition and targeted microbial interventions represent the frontier of metabolic disease
management.
CONCLUSION
The gut microbiome is a central player in the pathogenesis and potential treatment of diabetes and obesity.
Mechanistic insights into microbial regulation of host metabolism have paved the way for innovative therapeutic
strategies. A deeper understanding of microbial ecology, host genetics, and environmental influences will be
critical to fully harness the microbiome’s therapeutic potential in combating metabolic diseases.
REFERENCES
1. Chandrasekaran, P., Weiskirchen, R.: The Role of Obesity in Type 2 Diabetes Mellitus—An Overview.
International Journal of Molecular Sciences. 25, 1882 (2024). https://doi.org/10.3390/ijms25031882
2. Chellappan, D.K., Chellian, J., Rahmah, N.S.N., Gan, W.J., Banerjee, P., Sanyal, S., Banerjee, P., Ghosh,
N., Guith, T., Das, A., Gupta, G., Singh, S.K., Dua, K., Kunnath, A.P., Norhashim, N.A., Ong, K.H.,
Palaniveloo, K.: Hypoglycaemic Molecules for the Management of Diabetes Mellitus from Marine
Sources. DMSO. 16, 2187–2223 (2023). https://doi.org/10.2147/DMSO.S390741
https://www.eejournals.org Open Access
This is an Open Access article distributed under the terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the
original work is properly cited
Page | 49
3. Chen, B., Li, T., Wu, Y., Song, L., Wang, Y., Bian, Y., Qiu, Y., Yang, Z.: Lipotoxicity: A New Perspective
in Type 2 Diabetes Mellitus. Diabetes Metab Syndr Obes. 18, 1223 –1237 (2025).
https://doi.org/10.2147/DMSO.S511436
4. Ahmed, B., Konje, J.C.: The epidemiology of obesity in reproduction. Best Practice & Research Clinical
Obstetrics & Gynaecology. 89, 102342 (2023). https://doi.org/10.1016/j.bpobgyn.2023.102342
5. Uti, D.E., Alum, E.U., Atangwho, I.J., Ugwu, O.P.-C., Egbung, G.E., Aja, P.M.: Lipid-based nano-carriers
for the delivery of anti-obesity natural compounds: advances in targeted delivery and precision
therapeutics. Journal of Nanobiotechnology. 23, 336 (2025). https://doi.org/10.1186/s12951-025-03412-
z
6. Atangwho, I.J., Omang, W.A., Obeten, U.N., Udeozor, P.A., Agada, S.A., Bawa, I., Ogbu, C.O.: Cytokines
as key players in obesity low grade inflammation and related complications. Obesity Medicine. 54, 100585
(2025). https://doi.org/10.1016/j.obmed.2025.100585
7. Alum, E.U.: Metabolic memory in obesity: Can early-life interventions reverse lifelong risks? Obesity
Medicine. 55, 100610 (2025). https://doi.org/10.1016/j.obmed.2025.100610
8. Ejemot-Nwadiaro, R.I., Betiang, P.A., Basajja, M., Uti, D.E.: Obesity and Climate Change: A Two-way
Street with Global Health Implications. Obesity Medicine. 100623 (2025).
https://doi.org/10.1016/j.obmed.2025.100623
9. Edeh, F.O., Ainebyoona, C., Alum, E.U., Uti, D.E., Ugwu, O.P.-C., Alum, B.N.: Unveiling the microbial
orchestra: exploring the role of microbiota in cancer development and treatment. Discov Oncol. 16, 646
(2025). https://doi.org/10.1007/s12672-025-02352-2
10. Pickard, J.M., Zeng, M.Y., Caruso, R., Núñez, G.: Gut Microbiota: Role in Pathogen Colonization,
Immune Responses and Inflammatory Disease. Immunol Rev. 279, 70 –89 (2017).
https://doi.org/10.1111/imr.12567
11. Fujita, K., Matsushita, M., De Velasco, M.A., Hatano, K., Minami, T., Nonomura, N., Uemura, H.: The
Gut-Prostate Axis: A New Perspective of Prostate Cancer Biology through the Gut Microbiome. Cancers
(Basel). 15, 1375 (2023). https://doi.org/10.3390/cancers15051375
12. Kho, Z.Y., Lal, S.K.: The Human Gut Microbiome – A Potential Controller of Wellness and Disease.
Front. Microbiol. 9, (2018). https://doi.org/10.3389/fmicb.2018.01835
13. Dahiya, D., Nigam, P.S.: Antibiotic-Therapy-Induced Gut Dysbiosis Affecting Gut Microbiota—Brain
Axis and Cognition: Restoration by Intake of Probiotics and Synbiotics. Int J Mol Sci. 24, 3074 (2023).
https://doi.org/10.3390/ijms24043074
14. Fakharian, F., Thirugnanam, S., Welsh, D.A., Kim, W.-K., Rappaport, J., Bittinger, K., Rout, N.: The Role
of Gut Dysbiosis in the Loss of Intestinal Immune Cell Functions and Viral Pathogenesis.
Microorganisms. 11, 1849 (2023). https://doi.org/10.3390/microorganisms11071849
15. Craciun, C.-I., Neag, M.-A., Catinean, A., Mitre, A.-O., Rusu, A., Bala, C., Roman, G., Buzoianu, A.-D.,
Muntean, D.-M., Craciun, A.-E.: The Relationships between Gut Microbiota and Diabetes Mellitus, and
Treatments for Diabetes Mellitus. Biomedicines. 10, 308 (2022).
https://doi.org/10.3390/biomedicines10020308
16. Aggarwal, N., Kitano, S., Puah, G.R.Y., Kittelmann, S., Hwang, I.Y., Chang, M.W.: Microbiome and
Human Health: Current Understanding, Engineering, and Enabling Technologies. Chem Rev. 123, 31–
72 (2022). https://doi.org/10.1021/acs.chemrev.2c00431
17. Morrison, D.J., Preston, T.: Formation of short chain fatty acids by the gut microbiota and their impact
on human metabolism. Gut Microbes. 7, 189 –200 (2016).
https://doi.org/10.1080/19490976.2015.1134082
18. Nogal, A., Valdes, A.M., Menni, C.: The role of short-chain fatty acids in the interplay between gut
microbiota and diet in cardio -metabolic health. Gut Microbes. 13, 18972 12.
https://doi.org/10.1080/19490976.2021.1897212
19. Zhao, Q., Elson, C.O.: Adaptive immune education by gut microbiota antigens. Immunology. 154, 28–37
(2018). https://doi.org/10.1111/imm.12896
20. Gieryńska, M., Szulc-Dąbrowska, L., Struzik, J., Mielcarska, M.B., Gregorczyk-Zboroch, K.P.: Integrity
of the Intestinal Barrier: The Involvement of Epithelial Cells and Microbiota—A Mutual Relationship.
Animals (Basel). 12, 145 (2022). https://doi.org/10.3390/ani12020145
21. Di Vincenzo, F., Del Gaudio, A., Petito, V., Lopetuso, L.R., Scaldaferri, F.: Gut microbiota, intestinal
permeability, and systemic inflammation: a narrative review. Intern Emerg Med. 19, 275–293 (2024).
https://doi.org/10.1007/s11739-023-03374-w
22. Rowland, I., Gibson, G., Heinken, A., Scott, K., Swann, J., Thiele, I., Tuohy, K.: Gut microbiota functions:
metabolism of nutrients and other food components. Eur J Nutr. 57, 1 –24 (2018).
https://doi.org/10.1007/s00394-017-1445-8
23. Guzior, D.V., Quinn, R.A.: Review: microbial transformations of human bile acids. Microbiome. 9, 140
(2021). https://doi.org/10.1186/s40168-021-01101-1
This is an Open Access article distributed under the terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the
original work is properly cited
Page | 49
3. Chen, B., Li, T., Wu, Y., Song, L., Wang, Y., Bian, Y., Qiu, Y., Yang, Z.: Lipotoxicity: A New Perspective
in Type 2 Diabetes Mellitus. Diabetes Metab Syndr Obes. 18, 1223 –1237 (2025).
https://doi.org/10.2147/DMSO.S511436
4. Ahmed, B., Konje, J.C.: The epidemiology of obesity in reproduction. Best Practice & Research Clinical
Obstetrics & Gynaecology. 89, 102342 (2023). https://doi.org/10.1016/j.bpobgyn.2023.102342
5. Uti, D.E., Alum, E.U., Atangwho, I.J., Ugwu, O.P.-C., Egbung, G.E., Aja, P.M.: Lipid-based nano-carriers
for the delivery of anti-obesity natural compounds: advances in targeted delivery and precision
therapeutics. Journal of Nanobiotechnology. 23, 336 (2025). https://doi.org/10.1186/s12951-025-03412-
z
6. Atangwho, I.J., Omang, W.A., Obeten, U.N., Udeozor, P.A., Agada, S.A., Bawa, I., Ogbu, C.O.: Cytokines
as key players in obesity low grade inflammation and related complications. Obesity Medicine. 54, 100585
(2025). https://doi.org/10.1016/j.obmed.2025.100585
7. Alum, E.U.: Metabolic memory in obesity: Can early-life interventions reverse lifelong risks? Obesity
Medicine. 55, 100610 (2025). https://doi.org/10.1016/j.obmed.2025.100610
8. Ejemot-Nwadiaro, R.I., Betiang, P.A., Basajja, M., Uti, D.E.: Obesity and Climate Change: A Two-way
Street with Global Health Implications. Obesity Medicine. 100623 (2025).
https://doi.org/10.1016/j.obmed.2025.100623
9. Edeh, F.O., Ainebyoona, C., Alum, E.U., Uti, D.E., Ugwu, O.P.-C., Alum, B.N.: Unveiling the microbial
orchestra: exploring the role of microbiota in cancer development and treatment. Discov Oncol. 16, 646
(2025). https://doi.org/10.1007/s12672-025-02352-2
10. Pickard, J.M., Zeng, M.Y., Caruso, R., Núñez, G.: Gut Microbiota: Role in Pathogen Colonization,
Immune Responses and Inflammatory Disease. Immunol Rev. 279, 70 –89 (2017).
https://doi.org/10.1111/imr.12567
11. Fujita, K., Matsushita, M., De Velasco, M.A., Hatano, K., Minami, T., Nonomura, N., Uemura, H.: The
Gut-Prostate Axis: A New Perspective of Prostate Cancer Biology through the Gut Microbiome. Cancers
(Basel). 15, 1375 (2023). https://doi.org/10.3390/cancers15051375
12. Kho, Z.Y., Lal, S.K.: The Human Gut Microbiome – A Potential Controller of Wellness and Disease.
Front. Microbiol. 9, (2018). https://doi.org/10.3389/fmicb.2018.01835
13. Dahiya, D., Nigam, P.S.: Antibiotic-Therapy-Induced Gut Dysbiosis Affecting Gut Microbiota—Brain
Axis and Cognition: Restoration by Intake of Probiotics and Synbiotics. Int J Mol Sci. 24, 3074 (2023).
https://doi.org/10.3390/ijms24043074
14. Fakharian, F., Thirugnanam, S., Welsh, D.A., Kim, W.-K., Rappaport, J., Bittinger, K., Rout, N.: The Role
of Gut Dysbiosis in the Loss of Intestinal Immune Cell Functions and Viral Pathogenesis.
Microorganisms. 11, 1849 (2023). https://doi.org/10.3390/microorganisms11071849
15. Craciun, C.-I., Neag, M.-A., Catinean, A., Mitre, A.-O., Rusu, A., Bala, C., Roman, G., Buzoianu, A.-D.,
Muntean, D.-M., Craciun, A.-E.: The Relationships between Gut Microbiota and Diabetes Mellitus, and
Treatments for Diabetes Mellitus. Biomedicines. 10, 308 (2022).
https://doi.org/10.3390/biomedicines10020308
16. Aggarwal, N., Kitano, S., Puah, G.R.Y., Kittelmann, S., Hwang, I.Y., Chang, M.W.: Microbiome and
Human Health: Current Understanding, Engineering, and Enabling Technologies. Chem Rev. 123, 31–
72 (2022). https://doi.org/10.1021/acs.chemrev.2c00431
17. Morrison, D.J., Preston, T.: Formation of short chain fatty acids by the gut microbiota and their impact
on human metabolism. Gut Microbes. 7, 189 –200 (2016).
https://doi.org/10.1080/19490976.2015.1134082
18. Nogal, A., Valdes, A.M., Menni, C.: The role of short-chain fatty acids in the interplay between gut
microbiota and diet in cardio -metabolic health. Gut Microbes. 13, 18972 12.
https://doi.org/10.1080/19490976.2021.1897212
19. Zhao, Q., Elson, C.O.: Adaptive immune education by gut microbiota antigens. Immunology. 154, 28–37
(2018). https://doi.org/10.1111/imm.12896
20. Gieryńska, M., Szulc-Dąbrowska, L., Struzik, J., Mielcarska, M.B., Gregorczyk-Zboroch, K.P.: Integrity
of the Intestinal Barrier: The Involvement of Epithelial Cells and Microbiota—A Mutual Relationship.
Animals (Basel). 12, 145 (2022). https://doi.org/10.3390/ani12020145
21. Di Vincenzo, F., Del Gaudio, A., Petito, V., Lopetuso, L.R., Scaldaferri, F.: Gut microbiota, intestinal
permeability, and systemic inflammation: a narrative review. Intern Emerg Med. 19, 275–293 (2024).
https://doi.org/10.1007/s11739-023-03374-w
22. Rowland, I., Gibson, G., Heinken, A., Scott, K., Swann, J., Thiele, I., Tuohy, K.: Gut microbiota functions:
metabolism of nutrients and other food components. Eur J Nutr. 57, 1 –24 (2018).
https://doi.org/10.1007/s00394-017-1445-8
23. Guzior, D.V., Quinn, R.A.: Review: microbial transformations of human bile acids. Microbiome. 9, 140
(2021). https://doi.org/10.1186/s40168-021-01101-1
https://www.eejournals.org Open Access
This is an Open Access article distributed under the terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the
original work is properly cited
Page | 50
24. Enache, R.-M., Profir, M., Roşu, O.A., Creţoiu, S.M., Gaspar, B.S.: The Role of Gut Microbiota in the
Onset and Progression of Obesity and Associated Comorbidities. Int J Mol Sci. 25, 12321 (2024).
https://doi.org/10.3390/ijms252212321
25. Zhao, Y., Yang, H., Wu, P., Yang, S., Xue, W., Xu, B., Zhang, S., Tang, B., Xu, D.: Akkermansia
muciniphila: A promising probiotic against inflammation and metabolic disorders. Virulence. 15, 2375555.
https://doi.org/10.1080/21505594.2024.2375555
26. Conlon, M.A., Bird, A.R.: The Impact of Diet and Lifestyle on Gut Microbiota and Human Health.
Nutrients. 7, 17 (2014). https://doi.org/10.3390/nu7010017
27. Geng, J., Ni, Q., Sun, W., Li, L., Feng, X.: The links between gut microbiota and obesity and obesity
related diseases. Biomedicine & Pharmacotherapy. 147, 112678 (2022).
https://doi.org/10.1016/j.biopha.2022.112678
28. Xiong, R.-G., Zhou, D.-D., Wu, S.-X., Huang, S.-Y., Saimaiti, A., Yang, Z.-J., Shang, A., Zhao, C.-N., Gan,
R.-Y., Li, H.-B.: Health Benefits and Side Effects of Short-Chain Fatty Acids. Foods. 11, 2863 (2022).
https://doi.org/10.3390/foods11182863
29. Park, J.-E., Park, H.-Y., Kim, Y.-S., Park, M.: The Role of Diet, Additives, and Antibiotics in Metabolic
Endotoxemia and Chronic Diseases. Metabolites. 14, 704 (2024).
https://doi.org/10.3390/metabo14120704
30. Arnesen, E.K., Thorisdottir, B., Bärebring, L., Söderlund, F., Nwaru, B.I., Spielau, U., Dierkes, J., Ramel,
A., Lamberg-Allardt, C., Åkesson, A.: Nuts and seeds consumption and risk of cardiovascular disease, type
2 diabetes and their risk factors: a systematic review and meta-analysis. Food Nutr Res. 67,
10.29219/fnr.v67.8961 (2023). https://doi.org/10.29219/fnr.v67.8961
31. Umoru, G.U., Atangwho, I.J., David-Oku, E., Uti, D.E., De Campos, O.C., Udeozor, P.A., Nfona, S.O.,
Lawal, B., Alum, E.U.: Modulation of Lipogenesis by Tetracarpidium conophorum Nuts via SREBP-
1/ACCA-1/FASN Inhibition in Monosodium-Glutamate-Induced Obesity in Rats. Natural Product
Communications. 20, 1934578X251344035 (2025). https://doi.org/10.1177/1934578X251344035
32. Hsu, C., Schnabl, B.: The gut–liver axis and gut microbiota in health and liver disease. Nat Rev Microbiol.
21, 719–733 (2023). https://doi.org/10.1038/s41579-023-00904-3
33. Lucier, J., Mathias, P.M.: Type 1 Diabetes. In: StatPearls. StatPearls Publishing, Treasure Island (FL)
(2025)
34. Roy, S., Pokharel, P., Piganelli, J.D.: Decoding the immune dance: Unraveling the interplay between beta
cells and type 1 diabetes. Mol Metab. 88, 101998 (2024). https://doi.org/10.1016/j.molmet.2024.101998
35. Shemtov, S.J., Emani, R., Bielska, O., Covarrubias, A.J., Verdin, E., Andersen, J.K., Winer, D.A.: The
intestinal immune system and gut barrier function in obesity and aging. FEBS J. 290, 4163–4186 (2023).
https://doi.org/10.1111/febs.16558
36. Li, X., Atkinson, M.A.: The Role for Gut Permeability in the Pathogenesis of Type 1 Diabetes – A Solid
or Leaky Concept? Pediatr Diabetes. 16, 485–492 (2015). https://doi.org/10.1111/pedi.12305
37. Majumdar, S., Lin, Y., Bettini, M.L.: Host-microbiota interactions shaping T-cell response and tolerance
in type 1 diabetes. Front. Immunol. 13, (2022). https://doi.org/10.3389/fimmu.2022.974178
38. Latif, A., Shehzad, A., Niazi, S., Zahid, A., Ashraf, W., Iqbal, M.W., Rehman, A., Riaz, T., Aadil, R.M.,
Khan, I.M., Özogul, F., Rocha, J.M., Esatbeyoglu, T., Korma, S.A.: Probiotics: mechanism of action, health
benefits and their application in food industries. Front Microbiol. 14, 1216674 (2023).
https://doi.org/10.3389/fmicb.2023.1216674
39. Salles, B.I.M., Cioffi, D., Ferreira, S.R.G.: Probiotics supplementation and insulin resistance: a systematic
review. Diabetol Metab Syndr. 12, 98 (2020). https://doi.org/10.1186/s13098-020-00603-6
40. Ali, S., Hamayun, M., Siraj, M., Khan, S.A., Kim, H.-Y., Lee, B.: Recent advances in prebiotics:
Classification, mechanisms, and health applications. Future Foods. 12, 100680 (2025).
https://doi.org/10.1016/j.fufo.2025.100680
41. Yadegar, A., Pakpoor, S., Ibrahim, F.F., Nabavi-Rad, A., Cook, L., Walter, J., Seekatz, A.M., Wong, K.,
Monaghan, T.M., Kao, D.: Beneficial effects of fecal microbiota transplantation in recurrent Clostridioides
difficile infection. Cell Host Microbe. 31, 695–711 (2023). https://doi.org/10.1016/j.chom.2023.03.019
42. Schupack, D.A., Mars, R.A.T., Voelker, D.H., Abeykoon, J.P., Kashyap, P.C.: The promise of the gut
microbiome as part of individualized treatment strategies. Nat Rev Gastroenterol Hepatol. 19, 7–25
(2022). https://doi.org/10.1038/s41575-021-00499-1
43. Akhtar, M., Chen, Y., Ma, Z., Zhang, X., Shi, D., Khan, J.A., Liu, H.: Gut microbiota-derived short chain
fatty acids are potential mediators in gut inflammation. Anim Nutr. 8, 350–360 (2021).
https://doi.org/10.1016/j.aninu.2021.11.005
44. Perrone, P., D’Angelo, S.: Gut Microbiota Modulation Through Mediterranean Diet Foods: Implications
for Human Health. Nutrients. 17, 948 (2025). https://doi.org/10.3390/nu17060948
This is an Open Access article distributed under the terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the
original work is properly cited
Page | 50
24. Enache, R.-M., Profir, M., Roşu, O.A., Creţoiu, S.M., Gaspar, B.S.: The Role of Gut Microbiota in the
Onset and Progression of Obesity and Associated Comorbidities. Int J Mol Sci. 25, 12321 (2024).
https://doi.org/10.3390/ijms252212321
25. Zhao, Y., Yang, H., Wu, P., Yang, S., Xue, W., Xu, B., Zhang, S., Tang, B., Xu, D.: Akkermansia
muciniphila: A promising probiotic against inflammation and metabolic disorders. Virulence. 15, 2375555.
https://doi.org/10.1080/21505594.2024.2375555
26. Conlon, M.A., Bird, A.R.: The Impact of Diet and Lifestyle on Gut Microbiota and Human Health.
Nutrients. 7, 17 (2014). https://doi.org/10.3390/nu7010017
27. Geng, J., Ni, Q., Sun, W., Li, L., Feng, X.: The links between gut microbiota and obesity and obesity
related diseases. Biomedicine & Pharmacotherapy. 147, 112678 (2022).
https://doi.org/10.1016/j.biopha.2022.112678
28. Xiong, R.-G., Zhou, D.-D., Wu, S.-X., Huang, S.-Y., Saimaiti, A., Yang, Z.-J., Shang, A., Zhao, C.-N., Gan,
R.-Y., Li, H.-B.: Health Benefits and Side Effects of Short-Chain Fatty Acids. Foods. 11, 2863 (2022).
https://doi.org/10.3390/foods11182863
29. Park, J.-E., Park, H.-Y., Kim, Y.-S., Park, M.: The Role of Diet, Additives, and Antibiotics in Metabolic
Endotoxemia and Chronic Diseases. Metabolites. 14, 704 (2024).
https://doi.org/10.3390/metabo14120704
30. Arnesen, E.K., Thorisdottir, B., Bärebring, L., Söderlund, F., Nwaru, B.I., Spielau, U., Dierkes, J., Ramel,
A., Lamberg-Allardt, C., Åkesson, A.: Nuts and seeds consumption and risk of cardiovascular disease, type
2 diabetes and their risk factors: a systematic review and meta-analysis. Food Nutr Res. 67,
10.29219/fnr.v67.8961 (2023). https://doi.org/10.29219/fnr.v67.8961
31. Umoru, G.U., Atangwho, I.J., David-Oku, E., Uti, D.E., De Campos, O.C., Udeozor, P.A., Nfona, S.O.,
Lawal, B., Alum, E.U.: Modulation of Lipogenesis by Tetracarpidium conophorum Nuts via SREBP-
1/ACCA-1/FASN Inhibition in Monosodium-Glutamate-Induced Obesity in Rats. Natural Product
Communications. 20, 1934578X251344035 (2025). https://doi.org/10.1177/1934578X251344035
32. Hsu, C., Schnabl, B.: The gut–liver axis and gut microbiota in health and liver disease. Nat Rev Microbiol.
21, 719–733 (2023). https://doi.org/10.1038/s41579-023-00904-3
33. Lucier, J., Mathias, P.M.: Type 1 Diabetes. In: StatPearls. StatPearls Publishing, Treasure Island (FL)
(2025)
34. Roy, S., Pokharel, P., Piganelli, J.D.: Decoding the immune dance: Unraveling the interplay between beta
cells and type 1 diabetes. Mol Metab. 88, 101998 (2024). https://doi.org/10.1016/j.molmet.2024.101998
35. Shemtov, S.J., Emani, R., Bielska, O., Covarrubias, A.J., Verdin, E., Andersen, J.K., Winer, D.A.: The
intestinal immune system and gut barrier function in obesity and aging. FEBS J. 290, 4163–4186 (2023).
https://doi.org/10.1111/febs.16558
36. Li, X., Atkinson, M.A.: The Role for Gut Permeability in the Pathogenesis of Type 1 Diabetes – A Solid
or Leaky Concept? Pediatr Diabetes. 16, 485–492 (2015). https://doi.org/10.1111/pedi.12305
37. Majumdar, S., Lin, Y., Bettini, M.L.: Host-microbiota interactions shaping T-cell response and tolerance
in type 1 diabetes. Front. Immunol. 13, (2022). https://doi.org/10.3389/fimmu.2022.974178
38. Latif, A., Shehzad, A., Niazi, S., Zahid, A., Ashraf, W., Iqbal, M.W., Rehman, A., Riaz, T., Aadil, R.M.,
Khan, I.M., Özogul, F., Rocha, J.M., Esatbeyoglu, T., Korma, S.A.: Probiotics: mechanism of action, health
benefits and their application in food industries. Front Microbiol. 14, 1216674 (2023).
https://doi.org/10.3389/fmicb.2023.1216674
39. Salles, B.I.M., Cioffi, D., Ferreira, S.R.G.: Probiotics supplementation and insulin resistance: a systematic
review. Diabetol Metab Syndr. 12, 98 (2020). https://doi.org/10.1186/s13098-020-00603-6
40. Ali, S., Hamayun, M., Siraj, M., Khan, S.A., Kim, H.-Y., Lee, B.: Recent advances in prebiotics:
Classification, mechanisms, and health applications. Future Foods. 12, 100680 (2025).
https://doi.org/10.1016/j.fufo.2025.100680
41. Yadegar, A., Pakpoor, S., Ibrahim, F.F., Nabavi-Rad, A., Cook, L., Walter, J., Seekatz, A.M., Wong, K.,
Monaghan, T.M., Kao, D.: Beneficial effects of fecal microbiota transplantation in recurrent Clostridioides
difficile infection. Cell Host Microbe. 31, 695–711 (2023). https://doi.org/10.1016/j.chom.2023.03.019
42. Schupack, D.A., Mars, R.A.T., Voelker, D.H., Abeykoon, J.P., Kashyap, P.C.: The promise of the gut
microbiome as part of individualized treatment strategies. Nat Rev Gastroenterol Hepatol. 19, 7–25
(2022). https://doi.org/10.1038/s41575-021-00499-1
43. Akhtar, M., Chen, Y., Ma, Z., Zhang, X., Shi, D., Khan, J.A., Liu, H.: Gut microbiota-derived short chain
fatty acids are potential mediators in gut inflammation. Anim Nutr. 8, 350–360 (2021).
https://doi.org/10.1016/j.aninu.2021.11.005
44. Perrone, P., D’Angelo, S.: Gut Microbiota Modulation Through Mediterranean Diet Foods: Implications
for Human Health. Nutrients. 17, 948 (2025). https://doi.org/10.3390/nu17060948
https://www.eejournals.org Open Access
This is an Open Access article distributed under the terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the
original work is properly cited
Page | 51
CITE AS: Bwanbale Geoffrey David (2025). The Gut Microbiome in
Diabetes and Obesity: Mechanisms and Therapeutic Implications.
EURASIAN EXPERIMENT JOURNAL OF MEDICINE AND MEDICAL
SCIENCES, 6(3):44-51
This is an Open Access article distributed under the terms of the Creative Commons Attribution License
(http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the
original work is properly cited
Page | 51
CITE AS: Bwanbale Geoffrey David (2025). The Gut Microbiome in
Diabetes and Obesity: Mechanisms and Therapeutic Implications.
EURASIAN EXPERIMENT JOURNAL OF MEDICINE AND MEDICAL
SCIENCES, 6(3):44-51
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