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Deneshwary Balu*, Teh Soo Pheng, Mavis Soo Zi Qing, Heng Wei Kee, MZ Iqbal, Sajida Parveen, Syed Ghouse Mohiuddin, Sohail Aziz


A number of studies show that the risk of developing type-II diabetes is closely linked to the presence and duration of overweight as well as obesity. Indeed, 90% of individuals with type-II diabetes are either overweight or obese.[16] Lipid accumulation in obesity triggers a lowgrade inflammation that results from an imbalance between pro- and anti-inflammatory components of the immune system and act as the major underlying mechanism for the development of obesityassociated diseases, notably insulin resistance and type-II diabetes.[14] Obese adipose tissues (AT) shows hallmarks of chronic low-grade inflammation, which is believed to facilitate the development of insulin resistance.[1] Insulin resistance is defined as a decreased response of the peripheral tissues to insulin action. Individuals with insulin resistance are predisposed to developing type-II diabetes mellitus (T2DM). Increasingly, insulin resistance has been recognized as the integral feature of the so-called metabolic syndrome, which includes glucose intolerance, insulin resistance, obesity, hypertriglyceridemia, low HDL cholesterol, hypertension, and accelerated atherosclerosis.[2] The cluster of pathologies known as metabolic syndrome, including obesity, insulin resistance, type-II diabetes, and cardiovascular disease (CVD), has become one of the most serious threats to human health. The dramatic increase in the incidence of obesity in most parts of the world has contributed to the emergence of this disease cluster, particularly insulin resistance and type-II diabetes.[3] Obesity is commonly associated with insulin resistance and hyperinsulinemia and is a major risk factor for the development of type-II diabetes and cardiovascular disease.[5] Obesity is an epidemic, calling for innovative and reliable pharmacological strategies. ShK-186 shows that, a selective and potent blocker of the voltage-gated Kv1.3 channel, counteracts the negative effects of increased caloric intake in mice with a diet which rich in fat and fructose. ShK-186 reduced weight gain, adiposity and fatty liver, decreased blood levels of cholesterol, sugar, HbA1c, insulin and leptin and enhanced peripheral insulin sensitivity. These changes mimic the effects of Kv1.3 gene deletion. ShK-186 did not alter weight gain in mice on a chow diet, suggesting that the obesity inducing diet enhances sensitivity to Kv1.3 blockade.[13] There is a growing evidence that Fatty acid-induced β cell apoptosis shows a link between obesity and diabetes.[4] Peroxisome Proliferator Activated Receptors (PPARs) are members of the nuclear hormone receptor super family. Three subtypes are described: PPARa, PPARd and PPARg, encoded by different genes. PPARs form heterodimers with retinoic X receptors (RXR) and regulate transcription of various genes after binding to PPAR Response Elements (PPREs). PPARg is implicated in adipocyte differentiation 1±3 and regulates lipid and glucose homeostasis.[6] A higher body mass index (BMI) is a strong predictor of type-II diabetes (T2D), with a linear increase in diabetes risk across the whole spectrum of BMI. Although, diabetes risk is highest in obese people with BMI~30 kg/m2, a great proportion of future cases comes from the large population of overweight individuals with a BMI between 25 and 30 kg/m2. Recent national figures from the US and UK suggest that at least one third of the population is now overweight and another third (24% UK) is obese [with severe implications for the future burden of diabetes.[7] In contrast, obesity increases the risk of chronic age-related diseases, such as type-II diabetes, heart disease, osteoarthritis, certain types of cancer, and thus constitutes a major and rising global health problem.[8] Moreover, leptin treatment ameliorated type-II diabetes mellitus and resolved hypogonadism. This study has three unique features: (1) Firstly, it represents the only opportunity to study the effects of leptin in leptin-naive adults. (2) Secondly, it describes hormone replacement treatment of a genetic form of obesity in adults and thirdly, it addresses the effects of leptin replacement in the only individual identified with leptin-deficiency who has a diagnosis of type-II diabetes mellitus. (11). Prevalence of childhood obesity is increasing world widely. This development is accompanied by an increased prevalence of type-II diabetes mellitus.[15]

Keywords: Diabetes Mellitus, Physicians attitude, Obesity, type-II Diabetes Mellitus, patient Adherence.

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