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Diabetes mellitus is affecting human health all over the world. Both environmental and genetic factors are implicated in its pathogenesis. However, the primary of the factors are still debated. Biochemical mechanism(s) in pancreatic b-cell destructions rendering reduced insulin secretion is postulated to be associated with genetic variation and hence the present proposal was aimed to explore insulin secretory capacity (HOMA-%B), insulin sensitivity (HOMA-%S) and total antioxidant status (TAS) in subjects having parental history of type 2 diabetes mellitus (T2DM) and compared with their negative counterpart. In this cross-sectional study, 96 normoglycemic subjects were enrolled, among them 48 subjects (case) had parental history of T2DM, rest 48 without parental history of T2DM (controls). Blood glucose was measured by glucose oxidase method. Serum total cholesterol, triglycerides and high density lipoprotein (HDL) cholesterol were measured using Dimension®RxL max clinical chemistry system, and serum low density lipoprotein cholesterol (LDL) were calculated by Friedewald formula. Serum insulin was measured by enzyme linked immunosorbent assay. HOMA-%B, HOMA-%S and insulin resistance (HOMA IR) were assessed from fasting glucose and insulin using HOMA2 calculator. Total antioxidant status (TAS) was determined by spectrophotometric technique. Data were expressed as median (range) and Mann Whitney U test was performed to calculate statistical difference between groups using GraphPad Prism (6.02). P value < 0.05 was taken as level of significance. Median (range) of age (years) was 35.0 (30–50) and 36.5 (30–49) in case and controls respectively. Median (range) of fasting and 2hrs plasma glucose (mmol/L) was 4.9 (3.4–7.7) and 5.9 (4.4–10.6) in case and 4.9 (3.5–5.9) and 5.8 (3.8–7.8) in control respectively. Median (range) of fasting serum insulin (μIU/mL) was 16.1 (4.8–53.2) and 13.3 (2.5–46.3) in case and controls which showed statistical difference (p = 0.0134). HOMA-%B was significantly higher in case compared to control [179 (55–381) vs 98 (56–335), p = 0.001]. HOMA %S was significantly lower [49.3 (17.2–95.8) vs 60.2 (15.5–152.9), p = 0.0365] and HOMA IR was significantly higher [2.0 (1.0–5.8) vs 1.7 (0.7– 6.5), p = 0.0365] in case compared to control subjects with BMI ≤ 25 Kg/m². No significance difference was observed in TAS between case and control group [1296 (579 – 2164) vs 1549 (737 – 2690) μmol/L, p = 0.1330]. Data concluded that normoglycemic offspring of T2DM subjects had higher insulin secretory capacity as evidenced by absolute circulating insulin level and HOMA-%B as a measure of pancreatic b-cell secretion suggesting possible influence on heightened expression of related genes. The plausible mechanism(s) are yet to be identified. Similar levels of total antioxidant status (TAS) in the two groups preclude the oxidative stress involved in the process. Keywords: Antioxidant status, diabetes, insulinaemic, normoglycemic offspring. Title: Insulinemic and antioxidant status in normoglycemic subjects with parental history of type 2 diabetes mellitus Author: Md. Ehsanul Islam khan, Biplob Chandra Shil International Journal of Healthcare Sciences ISSN 2348-5728 (Online) Vol. 10, Issue 1, April 2022 - September 2022 Page No: 15-20 Publisher: Research Publish Journals Website: www.researchpublish.com Published date: 21-April-2022 DOI: https://doi.org/10.5281/zenodo.6475539 Download link (Source): https://www.researchpublish.com/papers/insulinemic-and-antioxidant-status-in-normoglycemic-subjects-with-parental-history-of-type-2-diabetes-mellitus, Research Publish Journals (Publisher), Website: www.researchpublish.com, {"references":["[1]\tKing H, Aubert RE, Herman WH. Global burden of diabetes, 1995-2025: prevalence, numerical estimates, and projections. Diab Care 1998; 21:1414-31.","[2]\tAtlas ID. International Diabetes Federation, Brussels, 2015.","[3]\tOldroyd J, Banerjee M, Heald A, Cruickshank K. Diabetes and ethnic minorities. Postgrad Medical J. 2005;81(958):486–490.","[4]\tAkter S, Rahman MM, Abe SK, Sultana P. Prevalence of diabetes and prediabetes and their risk factors among Bangladeshi adults: a nationwide survey. Diabetes Care 2014;37(1): 910.","[5]\tWild S, Roglic G, Green A, et al. Global prevalence of diabetes: estimates for the year 2000 and projections for 2030. Diab Care 2004;27:1047-52.","[6]\tKobberling J, Tillil H, Empirical risk figures for first-degree relatives of non-insulin dependent diabetics. In The Genetics of Diabetes Mellitus. Kobberling J, Tattersall R, Eds. London, Academic Press, 1982, p. 201–209.","[7]\tDeFronzo RA, Lilly Lecture 1987. the triumvirate: beta-cell, muscle, liver; a collusion responsible for NIDDM. Diabetes 1988; 37:667–687.","[8]\tPerseghin G, Ghosh S, Gerow K, Shulman GI. Metabolic defects in lean nondiabetic offspring of NIDDM parents: a cross-sectional study. Diabetes 1997;46:1001–1009.","[9]\tGroop L, Forsblom C, Lehtovirta M, Tuomi T, Karanko S, Nissen M, Ehrnstrom BO, Forsen B, Isomaa B, Snickars B, Taskinen MR. Metabolic consequences of a family history of NIDDM (the Botnia study): evidence for sex-specific parental effects. Diabetes 1996; 45:1585–1593.","[10]\tVaag A, Henriksen JE, Beck-Nielsen H. Decreased insulin activation of glycogen synthase in skeletal muscles in young non obese Caucasian first-degree relatives of patients with non-insulin-dependent diabetes mellitus. J Clin Invest1992; 89:782–788.","[11]\tVolk A, Renn W, Overkamp D, Mehnert B, Maerker E, Jacob S, Balletshofer B, Haring HU, Rett K. Insulin action and secretion in healthy, glucose tolerant first degree relatives of patients with type 2 diabetes mellitus: influence of body weight. Exp Clin Endocrinol Diabetes 1999;107:140–147.","[12]\tKahn CR. Banting Lecture: Insulin action, diabetogenes, and the cause of type II diabetes. Diabetes 1994; 43:1066–1084.","[13]\tWar ram JH, Martin BC, Krolewski AS, Soeldner JS, Kahn CR. Slow glucose removal rate and hyperinsulinemia precede the development of type II diabetes in the offspring of diabetic parents. Ann Intern Med 1990; 113:909–915.","[14]\tMartin B, Warram JH, Krolewski AJ, Bergman RN, Soeldner JS, Kahn CR. Role of glucose and insulin resistance in development of type 2 diabetes mellitus: result s of a 25-year follow-up study. Lancet 1992; 340: 925–929."]}