Research Article Integrative Obesity and Diabetes Integr Obesity Diabetes, 2017 doi: 10.15761/IOD.1000179 Volume 3(3): 1-4 ISSN: 2056-8827 Introduction Obesity is a complex trait caused by an excessive accumulation of adipose tissue and influenced by diet, developmental stage, age, physical activity and genetic makeup [1]. It is considered as a health disaster and the prevalence is increasing significantly in both developed and developing countries [2]. It results from an imbalance between food intake and energy expenditure causing an excessive accumulation of adipose tissue [3]. e prevalence of obesity worldwide is estimated to 500 million adults of which 1.5 million people are overweight or obese [4]. e body mass index (BMI) is used to define obesity, which will be defined as a BMI 30 kg/m 2  or greater as stated [5]. e most devastating outcome of obesity istype 2 diabetes mellitus (T2DM) as its prevalence is expected to increase from 171 million people at the start of this century to 360 million people by 2030 [5]. Insulin resistance is the common link associated with obesity and diabetes mellitus. It is due to decreased insulin-stimulated glucose transport and metabolism in adipocytes and skeletal muscle and by impaired suppression of hepatic glucose production. Pathologically various mechanisms contribute to the development of insulin resistance such as impaired insulin and insulin receptor interaction in the periphery, alteration in insulin signaling molecules like IRS 1 and 2, Protein kinase B (Akt), C, decreased expression of insulin receptors or translocation of glucose transporters (GLUT) [6]. Diabetes mellitus (DM) is a metabolic syndrome which alters carbohydrate, protein, fat and energy metabolism and is caused by the absence of insulin secretion or due to defects in insulin action in the peripheral tissue [7]. Inappropriate insulin production from pancreatic β-cells and peripheral insulin resistance are the two key factors T2DM pathogenesis[8]. Insulin resistance may result in elevated fatty acids in the plasma, decreased glucose transport into the muscle cells, and increased fat breakdown, which leads to higher hepatic glucose production. Despite insulin resistance being the common link between obesity and T2DM,all the obese subjects do not develop hyperglycemia due to insulin resistance as beta cells of Langerhans release appropriate Metabolic risk factors in obesity and diabetes mellitus: implications in the pathogenesis and therapy Vineet Kumar Khemka and Anindita Banerjee* ICARE Institute of Medical Sciences and Research, Haldia, West Bengal, India Abstract e increased prevalence of obesity worldwide is a serious problem as it invites several other metabolic chronic disorders including Diabetes mellitus, one of the major global pandemic now a days. Obesity raises the propensity of developing insulin resistance and type 2 diabetes mellitus (T2DM) by several folds. Adipose tissue derived increased amounts of non-esterified fatty acids, glycerol, hormones, proinflammatory cytokines and other factors are involved in the development of insulin resistance in obese individuals. When insulin resistance is accompanied by pancreatic islet β-cell dysfunction, glycemic control worsens resulting in diabetes. Abnormalities in β-cell function are therefore critical in defining the risk and development of type 2 diabetes. Although clinical studies aimed at reducing the deleterious effects of these conditions have been conducted or are undergoing trials, detailed exploration of the molecular and metabolic basis of the disease may guide us to new approaches to its prevention and treatment. amounts of insulin to maintain normal glucose tolerance. Moreover, endothelial dysfunction and nonesterified fatty acids (NEFAs) are also linked with obesity or insulin resistance in T2DM [9-11]. Studies in dogs suggest that it is the nocturnal elevations in NEFAs that might underlie the β-cell’s adaptive response to insulin resistance[12]. Elevated NEFA levels produced by a lipid infusion in vivo contribute to the development of insulin resistance and also prevent the expected compensatory β-cell response in humans[13]. is dual effect makes them a good candidate to link insulin resistance and β-cell dysfunction in individuals with type 2 diabetes and those at risk of the disorder. is lipotoxic effect can also act synergistically with glucose to produce even greater deleterious effects, commonly referred to as ‘glucolipotoxicity’. is review attempts to explore the metabolic risk factors associated with obesity and T2DM and their preventive management therapies. Risk factors in obesity and T2DM ere are multiple risk factors associated with obesity and diabetes mellitus which includes physical inactivity, sedentary lifestyle, family history, high risk ethnicity, cardiovascular disease (CVD), dyslipidemia, hypertension, sleep apnoea, renal disease, and others[14].  e gene polymorphisms in ADIPOQ (rs1501299 and rs17300539), LepR (rs1137101 and rs1045895), IRS2 (rs1805092), GRB14 (rs10195252 and rs3923113) and PPARG (rs1801282) have also been associated with overweight and obesity in uncontrolled T2DM [15]. Apart from the gene polymorphisms, population based long-term prospective and cross-sectional studies have identified many risk factors of T2DM as well as obesity, and some of these like altered blood levels of adipokines, chemokines, elevated circulating proinflammatory cytokines, vitamin Correspondence to: Anindita Banerjee, ICARE Institute of Medical Sciences and Research, Haldia, West Bengal, India-721645, Tel: +91-9830476354; E-mail: anny.banerjee@gmail.com Received: April 10, 2017; Accepted: May 08, 2017; Published: May 11, 2017