insulin resistance in pregnancy and early detection tool to detect iabetes and toxemia of pregnancy .drm surendra

in first trimester itself by checking serum insulin we need not wait upto 26 to 32 weeks to detect gesttional diabetes
09963721999

1. S CREENING AND MANAGEMENT OF GDM Presentation by DR.MUDDU SURENDRA NEHRU.M.D. @SURENDRA.MUDDU 09963721999

2. insulin resistance and pancreatic beta cell failure to secrete required amount of insulin ends upin diabetes. best example for physiological causes of insulin resistance is pregnancy. by screening every girl from age of 18 years for waist circumference above >85 cms, insulin resistance induced obesity leading to diabetes can be diagnosed and GDM complications can be prevented physical exercise,proper diet counselling,yoga, meditation helps in non-pharmacological management of GDM. following up the GDM group of patients for next 30 yeras ,diabetes, obesisity,heart and brain strokes,cancer can be prevented by HOMA-IR TEST. HBA1C IS HISTORY.FOR EVERY INDIAN woman with PREGNANCY ,FASTING INSULIN,KRAFT TEST IS COMPULSORY. GDM 09963721999 WWW.HOMASURENDRANEHRU.CO.IN

3. Introduction WITH OBESITY CROSSSING 75% OF WORLD POPULATION,AND INDIA BEING HIGHEST POPULATED COUNTRY ON EARTH,A NEW PROBLEM HAS ARISEN IN INDIA;OBESITY INDUCED INSULIN RESISTANCE COMPLICATING PREGNANCY.WITH RECENT TRENDS OF OBESITY IN GIRLS AND BOYS INCREASING,SOFTWARE BOOM,FOOD INDUSTRY RUNNING IN BILLION OF RUPEES,AND SLEEPLESSNESS TRIGGERED AWAVE OF OBE SITY INDUCED INSULIN RESISTANCE LEADING TO DIABETES Presentation by DR.M.SURENDRA NEHRU Page 04

4. adolescents-girls-normal cut off values WC=waist circumference>85 abnormal WHR-waist to hip ratio>0.8 abnormal WtHR-waist to height ratio>0.5-abnormal-best index BMI-body weight/body height squared ratio>kg/m2 <24-normal bmi 24-28 bmi-mild obese >28-30-high side of obesity >30-heavy obesity

5. obesity>M.S>IR IDF-INDIA-M.S-2 ENOUGH,ATP-3 1.WC>85 2.BP>130/90 3.TG>150/dl 4.FBS>100 5.HDL<40mg/dl PRE-DIABETES 1.IFG>FBS>100. 2.IGT>140 to 199 after 75gms glucose after 2 hours DIABETES 1.fbs>120 2.pprbs>2 hours>200mg/dl IR HOMA IR>2.5 cut off india adolescents

6. new markers high risk group for GDM new markers 1.prepartum BMI>28-30 2.FT-BMI>first trimester BMI>28 3 HOMA-IR.First trimester HOMA IR >2.5 4.VAI>visceral adiposity Index>higher the anterior abdominal wall of foetus> 5.normal BMI<24 with HOMA -IR>1.6 OR LESS THAN 2-indicates high risk for GDM 6.BMI>28 HOMA IR>3.5 OR ABOVE 2 IS highly indicative of GMS.GDM 7.QUICKI index<0.3 indicates high risk 8.Fasting Insulin >15.2 high risk group

7. HOMA-IR replace OGTT OGTT done during second trimester HOMA -IR is done in first trimester 24 to 26 weeks OGTT HBA1C is a failure HOMA-IR WITH 1.increased TYG INDEX 2.TYG-HDL INDEX 3.FT-BMI WITH HOMA IR 4.PREPARTUM BMI WITH HOMA IR 5.WC.WHR.WHtR AND HOMA IR predict highest GDM 6.fasting insulin >15 7.HOMA IR with high central obesity first trimester>88cms>WHR>0.88>high HOMA IR.HIGH INSULIN,LOW ADIPONECTIN>GDM HIGH 8.EARLY PREGNANCY with High HOMA -IR highrisk for GDM

8. glucose metabolism

9. Oral disposition index Heart of glucose management is oral disposition index When we eat our lunch The carbohydrates are absorbed and glucose enters blood stream The pancreas releases insulin in high quantity Insulin reduces blood sugar and after 2 hours insulin comes to normal level This mechanism is depicted on a mathematical order on a paper it is called oral disposition index The next few slides are about explaining ODI

10. Oral disposition index Oral disposition index as insulin clamp model is lab oriented And difficult in clinical arena Surrogate markers are developed to understand and prevent diabetes Concept is: Like oral glucose tolerance test patient under fasting 1.Zero -0 –minutes, glucose and insulin samples taken After 75mg of glucose orally given Samples collected for both glucose, insulin are taken at 30min,1 hour,2 hour,3,4,5 hours Insulin sensitivity to insulin units consumed are plotted

11. Overview Introduction Problem Literary Review Theoretical Framework Objectives Hypothesis Conclusion Methodology Thank You Implementation Result Page 03 MUDDU SURENDRA NEHRU

12. 1947 Low income poverty Govt,private sector,markets had no money Poverty due to failure to production of money T his is called poverty due to low production or low income poverty

13. 2022-high income poverty The poverty is due to failed distribution of money,or in equality Govt,markets,private sector has money Poverty is due to failure in income inequality This is called high income or high money economy with poverty

14. Normal insulin levels Fasting insulin is 3 to 15 miu/l 30 minutes after glucose -30 to 230 miu/l 1 hour after glucose-20 to 266 miu/l 2 hours after glucose-15 to 166 miu/l

15. Gestational diabetes (GDM) has emerged as the most common pregnancy complication affecting 7–17% of pregnancies worldwide ( 1 , 2 ), representing a growing, urgent public health concern ( 3 ). The increasing prevalence of GDM may be fueling the epidemic of adverse sequelae including type 2 diabetes and obesity among women and their offspring ( 4 ), forming a vicious intergenerational cycle ( 5 ). Moreover, GDM is conventionally screened for and diagnosed at the beginning of the third trimester, leaving little time for effective interventions or treatment, which has further galvanized the need for early identification of high-risk women for GDM. Obesity is a major risk factor for GDM ( 6 ). Notably, data are mostly on overall obesity defined based on body mass index (BMI); however, GDM is also frequently observed in women with normal BMI ( 7 ). Problem 1 Problems Presentation by Juliana Silva Page 05

16. Insulin receptor and signalling pathway Insulin binds to insulin receptor in the cell Insulin receptor has 2 proteins 1.SHC,IRS IRS stimulates P13K activates PIP3, PI3/AKT and MAPK pathways play important role in glucose absorption and ageing MTORC1 AND MTOR are useful in downstream signallin pathway Insulin resistance is hyperinsulinemia with post receptor signalling pathway failure

17. HOW TO MAKE OUT INSULIN RESISTANCE MODEL? Euglycemia with high insulin resistance Blood sugar is normal with fasting insulin levels more than 10 miu/ml Ty G INDEX -triglycerides to glucose ratio more than 4.3 HOMA -IR MORE THAN 2.3

18. gdm 01 According to the World Health Organization (WHO) and American Heart Association/National Heart, Lung, and Blood Institute recommendations on cutoff points for women, central obesity was defined as WHR ≥0.85 or WC ≥88 cm ( 24 ). ethnic specific cutoff points for WC (≥80 cm for non-Caucasians) according to the International Diabetes Federation and Adult Treatment Panel III recommendations in sensitivity analyses ( 25 , 26 ). Presentation by DR.M surendranehru Page 06 02 Recommendations are for screening for gestational diabetes at 24 to 28 weeks of pregnancy with a 50-g, 1-hour oral glucose challenge test. If the values are abnormal, greater than or equal to 130 mg/dL (7.22 mmol/L), or greater than or equal to 140 mg/dL (7.77 mmol/L), a confirmatory test is necessary with a 100-g, 3-hour oral glucose tolerance test, with the following values: first hour over 180 mg/dL, second hour over 155 mg/dL, third hour more than 140 mg/dL. The presence of two or more abnormal results establishes the diagnosis of gestational diabetes.

19. How to measure insulin resistance? 1.euglycemic-clamp-GOLD STANDARD .hyperinsulinemic clamp Insulin suppression test All the above tests invasive and not clinically easy to perform Surrogate tests 1.HOMA-IR 2.QUICKI-Quantitative insulin sensitivity check index 3.CIGMA-continuous infusion of glucose model assessment 4.IVGTT- with frequent insulin sampling

20. gdm established risk factors for GDM [i.e., age ≥35 years, minority race/ethnicity, prepregnancy overweight/obesity (BMI ≥23.0 kg/m2 for Asians or ≥25.0 kg/m2 for non-Asians), family history of diabetes, previous GDM, and pre-existing hypertension], Page 07 established risk factors of GDM:

21. Gestational diabetes managed without medication and responsive to nutritional therapy is diet-controlled gestational diabetes (GDM) or A1GDM. gestational diabetes managed with medication to achieve adequate glycemic control is A2GDM The definition of gestational diabetes mellitus (GDM) is any degree of glucose intolerance with onset or first recognition during pregnancy. GDM can classify as A1GDM and A2GDM. CLassification of GDM Page 08 Presentation by DR.M.SURENDRANEHRU

22. CRITERIA FOR GDM

23. CUT OFF LEVELS BLOOD SUGAR . A diagnosis of overt diabetes can be established in women who meet any of the following criteria: fasting plasma glucose level (FPG) ≥7.0 mmol/l (126 mg/dl), a casual plasma glucose of 11.1 mmol/l (≥200 mg/dl), or HbA1c ≥6.5 . Confirmation of the diagnosis precludes the need for OGTT. If FPG is >5.0 mmol/l (90 mg/dl) but <7.0 mmol/l (126 mg/dl) at any gestational age, a diagnosis of GDM can be made. If early screening is negative , the IADPSG recommends universal screening to be performed at 24-28 weeks of gestation with a 2-hour (h), 75-g OGTT “one-step approach”. Gestational diabetes is diagnosed, if one or more values equal, or exceeds thresholds; FPG (5.1 mmol/l [92 mg/dl]), one h plasma glucose (10 mmol/l [180 mg/dl]), and 2-h plasma glucose (8.5 mmol/l [153 mg/dl]). These cut-off values were chosen arbitrary by the IADPSG based on the HAPO study 17 HAPO Study Cooperative Research Group. Metzger BE, Lowe LP, Dyer AR, Trimble ER, Chaovarindr U, et al. Hyperglycemia and adverse pregnancy outcomes. N Engl J Med. 2008;358:1991–2002. [ PubMed ] [ Google Scholar ] [ Ref list ]

24. Gestational diabetes etiology is apparently related to 1) the pancreatic beta-cell dysfunction or the delayed response of the beta cells to the glycemic levels, and 2) the marked insulin resistance secondary to placental hormonal release. The human placental lactogen is the main hormone related to increased insulin resistance in GDM. Other hormones related to the development of this disease are growth hormone, prolactin, corticotropin-releasing hormone, and progesterone, these hormones contribute to the stimulation of insulin resistance and hyperglycemia in the pregnancy Hypothesis @muddusurendranehru 9963721999 Presentation by DR.M.SURENDRANEHRU Page 09

25. INSULIN RESISTANCE diabetes Failure of post receptor complex signalling Cells become deprived of glucose In Spite of high insulin levels in the body This is called ”insulin resistance “ hyper glycaemia, IGT, diabetes Seen in obese,sedentary,middle age group Due to insulin post receptor signalling failure

26. Diagnosing insulin resistance +insulin deficit diabetes? Using HOMA IR+HOMA B Majority of diabetes patients are in this category Starting metformin+sulfonylurea to insulin resistance patients Diabetic patients failing with 2 drug regimen requiring insulin Anydiabetic patient with glycemic deterioration

27. pathophysiology The human placental lactogen is a hormone released by the placenta during the pregnancy. It holds a comparable composition to growth hormone and induces important metabolic changes during pregnancy to support the maintenance of fetal nutritional status. This hormone is capable of provoking alterations and modifications in the insulin receptors. The following molecular variations appear to have links to diminishing glucose uptake at peripheral tissues:1) molecular alteration of the beta-subunit insulin receptor, 2) diminished phosphorylation of tyrosine kinase, 3) remodelings in the insulin receptor substrate-1 and phosphatidylinositol 3-kinase. Maternal high glucose levels cross the placenta and produce fetal hyperglycemia. The fetal pancreas gets stimulated in response to the hyperglycemia. Insulin anabolic properties induce fetal tissues to growth at an increased rate. [3] pathophysiology 01 02 Page 10

28. 3.combination model Insulin resistance with insulin deficit As the pancreas goes on pumping insulin Beta cells of pancreas gets exhausted leading to beta cell failure So,insulin resistance diabetes develops insulin deficit and is now called Insulin resistance with insulin deficient diabetes

29. The ADA recommends to consider screening strategy for detecting pregestational diabetes or early gestational diabetes mellitus in all women who are overweight or obese and have one or more of the following risk factors: Physical inactivity, First degree relative with diabetes High-risk race or ethnicity Have previously birthed an infant weighing 4000 grams or more Previously gestational diabetes, hypertension HDL level less than 35mg/dL Triglyceride level greater than 250 mg/dL Women with polycystic ovarian syndrome Hemoglobin A1c greater than 5.7% Impaired glucose tolerance test Impaired fasting glucose History of cardiovascular disease Other clinical conditions associated with insulin resistance Lorem ipsum dolor sit amet, consectetur adipiscing elit. Vivamus sed vestibulum nunc, eget aliquam felis. Phase 1 Phase 2 Implementation @muddusurendranehru9963721999 Presentation by DR.SURENDRANEHRU.MUDDU Page 11

30. WHY HBA1C IS HISTORY? The American Diabetes Association (ADA) has noted that measurement of hemoglobin A1C is usable, but it may not be suitable to use alone, due to decreased sensitivity compared to oral glucose tolerance test.

31. What is HOMA IR? Homeostasis model for assessment of insulin resistance formula=fasting insulin*fasting glucose/405 Normal value:is %.<1 is insulin sensitive Value more than 2.3 is taken as insulin resistance Fasting blood sugar may be normal

32. HOMA-B HOMA B CALCULATION= 20*(FASTING INSULIN mu/ML)/(FASTING BLOOD SUGAR mg/DL)-63 in metric units in mmol the formula=20*fasting insulin(mIu/ML/fasting glucose(mmol/ml)-3.5 GIVEN IN % LESS THAN 32% BETA CELL FAILURE CALCULATION

33. TY-G triglycerides to glucose index Ty-G index indicates high insulin insulin resistance TyG index formula= [fasting triglyceride(mg/dl)*fasting glucose(mg/dl)]/2 Cut off point is if above 4.3 it is taken as insulin resistance If 2 is within the backet it is 8.5 value Insulin plays a role in lipolysis prevention In insulin resistance the high insulin prevents the breakdown of lipids and increases hepatic lipogenesis,thereby triglycerides are increased

34. KRAFT TEST OGTT-WITH INSULIN ASSAY-FOR IR 75 gms of oral glucose is given in fasting state with samples taken for glucose and insulin Following glucose ,insulin,glucose is tested 30,60,120,180 min, and extended insulin tested upto 5 hours The patterns seen after are divided into 5 patterns based on time and quantity and time of insulin raise

35. .

36. MONITORING The ACOG recommended levels of blood glucose in pregnancy is fasting plasma glucose under 95 mg/dL, 1 hour postprandial under 130-140 mg/dL, 2 hours postprandial below 120mg/dL. In the postpartum period, 24 to 72 hours after the delivery, it is recommended to monitor glucose levels. After removing the placenta insulin resistance tends to improve, this can help escalate down insulin or hypoglycemic agents. Glycemic therapy will point towards achieving a euglycemic glucose level. At 4 to 12 weeks post-partum, it is recommended to perform a 75g oral glucose tolerance test to rule out the possibility of development of type 2 diabetes. [1][6][4][6] Presentation by DR.SURENDRANEHRU.MUDDU Page 12

37. monitoring glucose CGM 1.advantages less weight gain mother 2. more use of insulin 3.baby weight gain less 4.less HOMA IR SMBG- no difference in overall survival 2.no increase in complications HOMA ir controlled surgical decision same cheaper HBA1C <6 SMBG BEST

38. TREATMENT Gestational diabetes management begins with nonpharmacologic measurements like diet modifications, exercise, and glucose monitoring. The IDA recommends nutritional counseling by a registered dietitian and development of a personalized plan based on the patients BMI. In some settings, in which dietitians are not able, the physician can provide recommendations based on the three major nutritional concepts: caloric allotment, caloric distribution, and carbohydrate intake. 1.DIET.

39. breakfast >high carbohydrate load vs low carbs high carbohydrate in the morning better results less HOMA-IR 2.less mother weight GWG 3.baby less weight gain 4. disadvantage >highe GV>glycemic variability diet is the key in gdm 90% gdm managed with diet <50%carbohydrates ,3 meals,2 snacks,plus 1 snack at bed time

40. DIET weight gain in pregnancy-bmi ,<bmi<18 ,bmi-18 to 24 bmi >30 weight gain >12 kg weight gain allowed> 6 kgs <6 kg weight gain allowed bmi-18 to 24 bmi-24 to 28 bmi>30 30kcal/kg/day 25cal/kg/day ,15 kcal/kg/day

41. Ketone diet Why LDL-C cholesterol increases but weight loss happen in keto -diet?

42. Intermittent -fasting Intermittent fasting ,weight loss, ketosis, cholesterol

43. E-TRF Early time restricted feeding Circadian rhythm is used in the diet protocol Last dinner should b 7 pm last,for everyone Every trial has proved intermittent fasting works in hyperglycemia,diabetes Carbohydrates to be restricted to 25 to 50% that is 500gms to 1000gms/day Fibre in the diet needs to be more than 400 gms /day

44. ETRF Intermittent fasting-insulin resistance-dyslipidemia-euglycemia

45. treatment 1.tablet-is sleep Minimum sleeping hours is 8 hours SDB-sleep disturbed breathing Sleep defragmentation Sleep deprivation Increase catecholamines release Increase cortisol in the evening Increases obesity,insulin resistance and decreases insulin sensitivity

46. MANAGEMENT 2.EXERCISE: The amount of exercise recommended in GDM is 30 minutes of moderate-intensity aerobic exercise at least five days a week or a minimum of 150 minutes per week.

47. treatment tablet-exercise from 16 to 60 years 10000 steps minimum per day everyone must walk Exercise increases insulin sensitivity,reduces insulin resistance Weight reduction with increased insulin sensitivity is seen with exercise,than diet alone Exercise is the basic foundation in the management of hyperglycemia

48. Every step counts-APA-SB guidelines 1.Definition of sedentary <5000 steps per day= sedentary 2.5000 to 7500 steps=mild physical activity 3.7500 to 10000 steps=mild active physical activity 4.10000 steps=moderate physical activity 5.12500 steps per day=high activity Why?10000 steps? Only at 10000 steps insulin sensitivity increased,insulin resistance is reduced,B.P IS REDUCED,improved glucose

49. PHARMOCOLOGICAL: Insulin can help achieve an appropriate metabolic control, and it is added to the management if fasting blood glucose is greater or equal to 95 mg/dL, if 1-hour glucose level is greater or equal to 140 mg/dL, or if 2-hour glucose level is greater than 120 mg/dL. Basal insulin dose can be calculated using the patient’s weight formula, 0.2 units/kg/day. If the blood glucose level becomes elevated following a meal, rapid-acting insulin, or regular insulin can be prescribed before the meal, starting the dose with 2 to 4 units. In the first trimester, the total daily insulin requirement is 0.7 units/kg/day, in the second trimester it is 0.8 units/kg/day, and in the third trimester, it is 0.9 to 1.0 units/kg/day. The patient should divide the total daily dose of insulin into two halves; one half given as basal insulin at bedtime, and the other half divided between three meals and given as rapid-acting, or regular insulin before meals. Lispro and aspart have approval for usage in pregnancy. The short-acting insulin is associated with less hypoglycemia.

50. bed time insulin 50% basal insulin 50% meal time insulin basal insulin,LONG ACTING insulin analog,NPH, REGULAR, RAPID ACTING aspart, dose and distribution of insulin during GDM dosage schedule-

51. insulin dosage 0.2 units/kg/day for starting>fbs>95 at bed time <bmi less than 24> insulin requirement is 0.2units/kg/day bmi>30- insulin dosage 1.5 units/kg/day first trimester-insulin dose.>0.7units/kg/day second trimester insulin dose>0.8units/kg/day third trimester - insulin dose >0.9 to 1.0 units/kg/day basal and meal scheme insulin is 50% basal long acting insulin at bedtime with 4 doses of rapid acting insulin 4 times postprandial blood sugar is more important than fbs in fetal outcomes, insulin glargine not yet fda approved.insulin detemir used,no data on insulin glulisine

52. MEDICINES: TABLETS The oral hypoglycemic agents, metformin and glyburide, are increasingly being used among women with gestational diabetes, despite the lack of FDA approval. Glyburide can initiate at a dose of 2.5 mg, and the maximum dose is 20mg. Metformin therapy should start at a dose of 500 mg, and the maximum dose is 2500 mg.

53. metformin,glibenclamide-gdm cost wise cheap for long distance villagers good people with no knowledge of insulin injections good glibenclamide better results than insulin for fetal anomalies reduction. failure rate-glibenclamide>20%.metformin>40% glibenclamide starting dose>2.5mg at morning, total dose max>20 mg failure is fbs>115mg Metformin class b drug>no maternal hypoglycemia,no evidence of fetal toxicity, 500mg starting dose,max>2500mg ACOG adapted oha,us fda approval pending

54. in hospital-intrapartum insulin dose and schedule blood sugar should be between-72 to 126mg/dl>best results Flores-le Roux JA, Sagarra E, Benaiges D, Hernandez-Rivas E, Chillaron JJ, Puig de Dou J, et al. A prospective evaluation of neonatal hypoglycaemia in infants of women with gestational diabetes mellitus. Diabetes Res Clin Pract. 2012;97:217–222. [PubMed] [Google Scholar] [Ref list] ivf-DNS at 125cc/hour,>NS>RL>GOAL>rbs should not cross 140mg/dl no specific dose, management based on SMBG, every 2 hours

55. postpartum-management 3 days hospital stay compulsory <fbs<125 mg/dl >after 6 weeks OGTT FBS>125>RBS>200 >1.DIET.2.EXERCISE.3.SLEEP.4.MEDICINES METFORMIN.GLIBENCLAMIDE CAN BE GIVEN DURING BREASTFEEDING. Glueck CJ, Wang P. Metformin before and during pregnancy and lactation in polycystic ovary syndrome. Expert Opin Drug Saf. 2007;6:191–198. [ PubMed ] [ Google Scholar ] [ Ref list ] Blumer I, Hadar E, Hadden DR, Jovanovič L, Mestman JH, Murad MH, et al. Diabetes and pregnancy: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2013;98:4227–4249. [ PMC free article ] [ PubMed ] [ Google Scholar ] [ Ref list ]

56. COMPLICATIONS The complications of developing gestational diabetes categorize as maternal and fetal. The fetal complications include macrosomia, neonatal hypoglycemia, polycythemia, shoulder dystocia, hyperbilirubinemia, neonatal respiratory distress syndrome, increased perinatal mortality, and hypocalcemia. Maternal complications include hypertension, preeclampsia, increased risk of developing diabetes mellitus, and increased risk of cesarean delivery. [12][13]

57. The management and treatment of women with gestational diabetes is an emerging challenge for health care providers and teams. Thus, today, gestational diabetes requires an interprofessional team approach, including physicians, specialists, specialty-trained nurses, and pharmacists, all collaborating across disciplines to achieve optimal patient results and prevent further complications. Efforts and strategies are necessary to recognize them effectively. The development of prevention strategies would facilitate the treatment of gestational diabetes and would help improve health outcomes. Women with gestational diabetes have an increased risk of developing type 2 diabetes over 10 to 20 years after pregnancy. [14][13][11][4] Many pregnant women who develop diabetes are not diagnosed until very late, which significantly increases the morbidity of the disease. Conclusion @muddusurendranehru 9963721999 Presentation by DR.M.SURENDRANEHRU Page 13

58. Thank You! Presentation by HOMA MUDDU SURENDRANEHRU @muddusurendranehru 9963721999 DR. SURENDRA NEHRU.MUDDU

59. References 1. Coustan DR. Gestational diabetes mellitus. Clin Chem. 2013 Sep;59(9):1310-21. [ PubMed ] 2. Jawad F, Ejaz K. Gestational diabetes mellitus in South Asia: Epidemiology. J Pak Med Assoc. 2016 Sep;66(9 Suppl 1):S5-7. [ PubMed ] 3. Spaight C, Gross J, Horsch A, Puder JJ. Gestational Diabetes Mellitus. Endocr Dev. 2016;31:163-78. [ PubMed ] 4. ACOG Practice Bulletin No. 190: Gestational Diabetes Mellitus. Obstet Gynecol. 2018 Feb;131(2):e49-e64. [ PubMed ] 5. Law KP, Zhang H. The pathogenesis and pathophysiology of gestational diabetes mellitus: Deductions from a three-part longitudinal metabolomics study in China. Clin Chim Acta. 2017 May;468:60-70. [ PubMed ] 6. Mack LR, Tomich PG. Gestational Diabetes: Diagnosis, Classification, and Clinical Care. Obstet Gynecol Clin North Am. 2017 Jun;44(2):207-217. [ PubMed ] 7. Chiefari E, Arcidiacono B, Foti D, Brunetti A. Gestational diabetes mellitus: an updated overview. J Endocrinol Invest. 2017 Sep;40(9):899-909. [ PubMed ] 8. Brzozowska M, Bieniek E, Szosland K, Lewinski A. Gestational diabetes - is diet and insulin the only solution? Neuro Endocrinol Lett. 2017 Oct;38(5):311-315. [ PubMed ] 9. Zheng J, Wang H, Ren M. Influence of exercise intervention on gestational diabetes mellitus: a systematic review and meta-analysis. J Endocrinol Invest. 2017 Oct;40(10):1027-1033. [ PubMed ] 10. Alfadhli EM. Gestational diabetes mellitus. Saudi Med J. 2015 Apr;36(4):399-406. [ PMC free article ] [ PubMed ] 11. Zhu Y, Zhang C. Prevalence of Gestational Diabetes and Risk of Progression to Type 2 Diabetes: a Global Perspective. Curr Diab Rep. 2016 Jan;16(1):7. [ PMC free article ] [ PubMed ] 12. Senat MV, Deruelle P. [Gestational diabetes mellitus]. Gynecol Obstet Fertil. 2016 Apr;44(4):244-7. [ PubMed ] 13. Lindsay RS, Mackin ST, Nelson SM. Gestational diabetes mellitus-right person, right treatment, right time? BMC Med. 2017 Aug 28;15(1):163. [ PMC free article ] [ PubMed ] 14. Ashwal E, Hod M. Gestational diabetes mellitus: Where are we now? Clin Chim Acta. 2015 Dec 07;451(Pt A):14-20. [ PubMed ]

60. RESUME

61. NAME :MUDDU SURENDRA NEHRU

62. QUALIFICATION :M.D.GENERAL MEDICINE

63. DATE OF BIRTH :06-02-1964

64. M.B.B.S STUDY :1981-1986

65. M.D. STUDY :1989-1992

66. PLACE OF STUDY :KURNOOL MEDICAL COLLEGE

67. POST-M.D :25 YEARS

68. WORKED AS :ASSISTANT PROFESSOR OF MEDICINE

69. DURATION OF WORK :8 YEARS

70. INSTITUTION WORKED :OSMANIA MEDICAL COLLEGE,OSMANIA GENERAL HOSPITAL

71. PRESENT DESIGNATION :M.D. SURENDRA NEHRU HOSPITAL GODAVARIKHANI

72. ACADEMIC ACTIVITIES :AUTHOR OF BOOK”TMT BASICS “( PARAS BOOK PUBLISHERS)

73. CO-AUTHOR WITH DR RAGHU “CVMETABOLIC DISORDERS”