Diabetes Mellitus both Type 1 and Type 2 ppt.pptx

Made ppt from lippincott biochemistry book
Purely from the biochemistry book
These ppt especially for the students of Biochemistry and Biotechnology

1. Diabetes Mellitus Presented By : Group 04 Maaz -012 Nazia Yousaf -014 Malaika Arshad -019 Sidra Noor -022 Sufyan Gohar -024 Eman Fatima -027 1

2. Content 2 2. Type 2 DM Introduction to Diabetes Mellitus 1. Type 1 DM Diagnosis of T1D Metabolic Changes in T1D Treatment of T1D Insulin Resistance in T2D Dysfunctional β Cells in T2D Metabolic Changes in T2D Treatment of T2D

3. 3 Causes of Diabetes Mellitus Diabetes mellitus (“diabetes”) is not one disease, but rather is a heterogeneous group of multifactorial, polygenic syndromes characterized by an elevated fasting blood glucose (FBG) caused by a relative or absolute deficiency in insulin. What is Diabetes Mellitus? Diabetes is the leading cause of adult. B lindness and amputation and a major cause of renal failure . Nerve damage Heart attacks Strokes.

4. 4 There are two types of Diabetes Mellitus Type 1 DM Type 2 DM 1. Type 1 DM Types of Diabetes Mellitus The disease is characterized by an absolute deficiency of insulin caused by an autoimmune attack on the β cells of the pancreas

5. 5 Contd. 1. Insulitis and β-Cell Destruction : In T1D, the islets of Langerhans in the pancreas are infiltrated by activated T lymphocytes, resulting in insulitis. This autoimmune attack gradually depletes the population of β cells over a period of years. 2. Environmental and Genetic Factors : β-cell destruction in T1D requires both an environmental stimulus, such as a viral infection, and a genetic determinant. The genetic determinant allows β cells to be recognized as " nonself " by the immune system, triggering the autoimmune response. 3. Difference from Type 2 Diabetes (T2D) : Unlike T2D, where the genetic influence is stronger, T1D has a less deterministic genetic influence. For example, among identical twins, if one twin develops T1D, the other twin has only a 30%–50% chance of developing the disease. In contrast, in T2D, virtually all identical twins eventually develop the disease.

6. 6 Contd. Typical Onset and Symptoms : T1D typically manifests during childhood or puberty. P olyuria (frequent urination), polydipsia (excessive thirst), and polyphagia (excessive hunger), These symptoms are often accompanied by fatigue and weight loss. Diagnostic Criteria : Diagnosis is confirmed by specific laboratory tests: Glycosylated hemoglobin (HbA1c) concentration Fasting Blood Glucose (FBG). Fasting is defined as no caloric intake for at least 8 hours. A random blood glucose level. Testing Methods : Diagnosis can be made through various tests: Fasting Blood Glucose (FBG) test. Oral Glucose Tolerance Test (OGTT) A . Diagnosis of type 1 diabetes

7. 7 Contd. The metabolic abnormalities of T1D mellitus result from a deficiency of insulin that profoundly affects metabolism in three tissues: liver, muscle, and adipose B . Metabolic changes in type 1 diabetes 1 . Hyperglycemia and ketoacidosis Hallmarks of Untreated T1D: Causes of Hyperglycemia: Causes of Ketosis: Diabetic Ketoacidosis (DKA) :

8. 8 Contd. Excess Fatty Acids: Formation of VLDLs: Chylomicron Synthesis: Lipoprotein Degradation: 2 . Hypertriacylglycerolemia :

9. 9 Contd. Reliance on Exogenous Insulin : Therapeutic Regimens : Standard Treatment: Injection Frequency : Blood Glucose and HbA1c Levels: Intensive Treatment: Monitoring and Injections: Blood Glucose and HbA1c Levels: Euglycemia : Reduction in Complications : C. Treatment of Type 1 Diabetes:

10. 10 Contd. Hypoglycemia in Type 1 Diabetes: Therapeutic Goals: Common Complication: Compensatory Mechanisms: Progression and Vulnerability: Impact of Exercise: Contraindications for Tight Control: Risks in Children: Risks in Elderly: Target Population for Tight Control :

11. 11 Prevalence : Gradual Onset: Common Symptoms : Pathophysiology: Insulin Resistance and β-Cell Dysfunction: Metabolic Alterations: Diagnosis : Pathogenesis : Non-Autoimmune Nature: Acute Complications: Hyperosmolar Hyperglycemic State (HHS): 2. Type 2 Diabetes

12. 12 Contd. Definition : Characterization : 1. Insulin Resistance and Obesity: Obesity as a Major Cause: Compensation Mechanism: Effectiveness of Compensation : A. Insulin Resistance:

13. 13 Contd. 2 . Insulin Resistance and Type 2 Diabetes: Dual Factors in T2D Development : Risk Factors for Insulin Resistance: Inadequate Compensation: Causes of Insulin Resistance: Impact of Weight Changes: Adipose Tissue as a Secretory Organ: Proinflammatory Secretions: Proinflammatory Cytokines : Leptin: Adiponectin Effects of Insulin Resistance: Increased Lipolysis Glucose Utilization Hepatic Steatosis : Proinflammatory Effects: Role of Adiponectin:

14. 14 Contd. Initial β-Cell Capacity : Progressive Dysfunction : Natural Progression of T2D : Acceleration of β-Cell Dysfunction : Deterioration of β-cell function can be accelerated by: Sustained Hyperglycemia Elevated Free Fatty Acids (FFAs ): Proinflammatory Environment : B. Dysfunctional β Cells in Type 2 Diabetes :

15. 15 Contd. Insulin Resistance : Metabolic Abnormalities: Hyperglycemia : Causes: Ketosis: Dyslipidemia : Fatty Acid Conversion: VLDL and Chylomicrons: Lipoprotein Degradation: HDL Levels: C. Metabolic Changes in Type 2 Diabetes :

16. 16 Contd. Treatment Goals : Lifestyle Modifications: Weight Reduction: Exercise : Medical Nutrition Therapy (Dietary Modifications): Pharmacological Treatments: Hypoglycemic Agents : Metformin: Sulfonylureas: Thiazolidinediones (TZDs): α- Glucosidase Inhibitors : Insulin Therapy : Surgical Treatment : D. Treatment of Type 2 Diabetes :

17. THANK YOU! Google Pictures: Lippincott Biochemistry 6 th Edition Reference :