Association of Serum Leptin with Beta Cell Dysfunction and Insulin Resistance among Different Subgroups of Prediabetes Israt Ara Hossain 1* , Mijanur Rahman Shah 2 , Fatema Jebunnesa 1 , Rahelee Zinnat 1 and Liaquat Ali 1 1 Department of Biochemistry and Cell Biology, Bangladesh University of Health Sciences, Dhaka, Bangladesh 2 Department of Microbiology and Immunology, Bangabandhu Sheikh Mujib Medical University, Dhaka, Bangladesh * Corresponding author: Israt Ara Hossain, Department of Biochemistry and Cell Biology, Bangladesh University of Health Sciences, Dhaka, Bangladesh, Tel: +88-02-9010654, Fax: +88-02-8055312; E-mail: israt.ru84@buhs.ac.bd Received date: May 03, 2019; Accepted date: June 21, 2019; Published date: June 28, 2019 Copyright: © 2019 Hossain IA, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Background: Accumulating evidence indicates that various adipokines released from adipose tissue have been involved in abnormal insulin signalling in obesity and type 2 diabetes. However, it is not entirely clear whether these alterations in serum adipocyte concentrations are already present in the prediabetic state. The present study was designed to test the hypothesis that elevated levels of serum lepin an index of insulin sensitivity is independently associated with insulinemic indices among different subgroups of prediabetes. Materials: Under an observational cross-sectional design a total of 116 Control subjects (M/F, 58/58) and 99 prediabetic subjects (55/44) consisting of 49 Impaired Fasting Glucose (IFG) and 50 Impaired Glucose Tolerance (IGT) were investigated. Serum glucose was measured by glucose-oxidase method. Serum insulin and leptin were measured by ELISA techniques. Insulin secretory function (HOMA%B), insulin sensitivity (HOMA%S) and Homeostasis Model Assessment-insulin resistance (HOMA-IR) were calculated from Homeostasis Model Assessment (HOMA). Results: Compared to the Control, IFG and IGT subjects had significantly higher levels of serum leptin (ng/mL) (p<0.001) and HOMA-IR (p=0.001) respectively. However, compared to their Control counterparts, IFG and IGT subjects had significantly lower levels of HOMA%B (p=0.001) and HOMA%S (p=0.010). On binary logistic regression analysis, serum leptin [OR (95% CI): 1.074 (1.019-1.131), p=0.007] and reduced HOMA%S [OR (95% CI): 0.972 (0.950-0.995), p=0.015] were found to be significant determinants of IGT group after adjusting the effects of WC and TG. In the same analysis, serum leptin [1.109 (1.054-1.167), p<0.001] and reduced HOMA%B [0.966 (0.951-0.981), p<0.001] were found to be significant predictors of IFG group after adjusting the effects of WC and TG. Conclusion: Elevated levels of serum leptin may have an association with the state of IFG and IGT of pre- diabetes and this association, in turn, is mediated by insulin secretory dysfunction and reduced insulin sensitivity during this disorder. Keywords: Leptin; Prediabetes; IFG; IGT; HOMA%B; HOMA%S; HOMA-IR Introduction Prediabetes the prior state of type 2 diabetes mellitus is a hyperglycemic condition that is characterized by Impaired Fasting Glycaemia (IFG), Impaired Glucose Tolerance (IGT) and combination of both defects (IFG-IGT) [1]. Prior clinical and epidemiological studies reveal both insulin resistance and insulin secretory dysfunction considered as the pathophysiologic determinants of hyperglycemia among prediabetes [2,3]. Obesity in association with insulin resistance and the components of metabolic syndrome manifests as the causative factors of prediabetes [4]. Adipose tissue in addition to its pathological and physiological action of the body it provides a link between obesity and insulin resistance where it acts as an active endocrine and paracrine organ, secreting a large number of biologically active compounds that involved in the metabolic homeostasis, collectively called adipokines [5]. Leptin, a 167 amino acid containing adipokine derived from adipocyte, which under normal physiological conditions regulate feeding behavior, energy expenditure, adipose tissue mass, facilitate glucose utilization and alters insulin secretion [6]. It plays a functional role in glucose homeostasis through its efects on the synthesis of insulin which also the risk factors for the development of prediabetes. Leptin inhibits the synthesis of insulin by inhibiting the pre-proinsulin mRNA expression in β cells. By activation of ATP-sensitive potassium channels leptin reduces the secretion of insulin from pancreatic β cells leading to the development of type 2 DM. Te exact mechanism whereby elevated levels of serum leptin predispose to prediabetes is still unknown. During obesity, lipotoxicity occurs in the extrahepatic tissues which in turn suppress the responsiveness of non-adipose tissues to the insulin thereby inhibiting the glucose uptake and its subsequent disposal into the hepatocytes. It was suggested that insulin resistance to leptin in the β-cells during glucose intolerant state, might prevent the inhibitory efect of leptin on insulin secretion resulting in hyperinsulinemia, which might exhaust pancreatic β-cells leading to the development of hyperglycemia. Journal of Diabetes and Metabolism Hossain et al., J Diabetes Metab 2019, 10:5 Research Article Open Access J Diabetes Metab, an open access journal ISSN: 2155-6156 Volume 10 • Issue 5 • 1000828