DAIBETES AND OBESITYIn today’s fast moving world, the desire to become successful and wealthy has made health a second fiddle. This has caused a significant rise in the number of diseases in our society.  Lack of healthy diet, increased intake of carbohydrates, lack of exercise and leading a sedentary lifestyle has caused an increase in the number of individuals becoming obese. Obesity is defined as increase in the overall deposition of fat over 20% of the normal weight of an individual. A BMI ( body mass index) of 25.9-29 is considered to be overweight and BMI over 30 is considered to be obese. Apart from being a cause of  life threatening diseases such as Hypertension, Coronary artery disease, Hyperlipidaemia, GERD, stroke, infertility; obesity is also a major cause of Type II diabetes mellitus.Diabetes Mellitus is defined as a chronic disease marked by increased blood sugar level. It is classified into two types i.e. Type I diabetes mellitus (insulin dependant) and Type II diabetes mellitus ( non insulin dependant). Type I diabetes mellitus is has hereditary  as it main etiology whereas Type II diabetes mellitus is a multifactorial disease with obesity, age, sex, race, environmental factors, genetic predisposition, culture, economic status being it’s main causes. Currently, 246 million people worldwide are suffering from this disease and this number is expected to rise to 380 million by the year 2025. The main symptoms of Type II diabetes mellitus are: I. Increase blood glucoseII. PolydypsiaIII. PolyuriaIV. Blurry visionV. FatigueVI. Impaired wound healingVII. NauseaIn type 2 diabetes, the body does not use insulin properly. This is called insulin resistance. At first, the pancreas makes extra insulin to make up for it. But, over time the pancreas isn’t able to keep up and can’t make enough insulin to keep the blood glucose levels normal, leading to a rise in blood glucose levels. When glucose builds up in the blood instead of getting utilised in the cells, it causes two main problems: the cells may be starved for energy due to lack of glucose utilisation and over time, high blood glucose levels damage the kidneys, heart, eyes , liver and many other major endocrinal functions of the body.Insulin resistance together with obesity lead to beta cell decompensation  in the pancrease leading to impaired production of insulin. Recent studies have identified “links” between obesity and type 2 diabetes involving proinflammatory cytokines (tumor necrosis factor and interleukin-6), insulin resistance, deranged fatty acid metabolism, and cellular processes such as mitochondrial dysfunction and endoplasmic reticulum stress. These interactions are complex, with the relative importance of each unclear. Mechanisms of obesity-associated insulin resistance:  The influence of obesity on type 2 diabetes risk is determined not only by the degree of obesity but also by where fat accumulates. Increased upper body fat including visceral adiposity, as reflected in increased abdominal girth or waist-to-hip ratio, is associated with the metabolic syndrome, type 2 diabetes, and cardiovascular disease, although underlying mechanisms remain uncertain. At least three distinct mechanisms have been proposed to link obesity to insulin resistance and predispose to type 2 diabetes: 1) increased production of adipokines/cytokines, including tumor necrosis factor-a, resistin, and retinol-binding protein 4, that contribute to insulin resistance as well as reduced levels of adiponectin; 2) ectopic fat deposition, particularly in the liver and perhaps also in skeletal muscle, and the dysmetabolic sequelae; and 3) mitochondrial dysfunction, evident by decreased mitochondrial mass and/or function. Mitochondrial dysfunction could be one of many important underlying defects linking obesity to diabetes, both by decreasing insulin sensitivity and by compromising ?-cell function.Mechanisms of progressive ?-cell dysfunctionin obese individuals: The link between obesity and hyperinsulinemia, reflects compensation by insulin-secreting ?-cells to systemic insulin resistance. Although mechanisms underlying this coupling (e.g., mild hyperglycemia and raised levels of circulating free fatty acids) remain elusive, obese normoglycemic individuals have both increased ?-cell mass and function. Obesity-induced glucose intolerance reflects failure to mount one or more of these compensatory responses. Factors predisposing to ?-cell decompensation could also be primarily genetic or epigenetic. A clear, mechanistic basis for this decompensation has remained elusive.Genetic factors linking obesity and diabetes : Genome-wide association scans (GWAS) and candidate gene approaches now have identified ~ 40 genes associated with type 2 diabetes and a similar number, albeit largely different, with obesity. Most type 2 diabetes genes appear to be related to ?-cell dysfunction, with many fewer involved in pathways related to insulin resistance independent of obesity. Many obesity gene variants appear to be involved in pathways affecting energy homeostasis. Although numerous diabetes- and obesity-associated genes have been identified, the known genes are estimated to predict only 15% of type 2 diabetes and 5% of obesity risk.Although the link between obesity and type 2 diabetes is widely held to involve two discrete lesions-obesity-induced insulin resistance and ? cell failure-both disorders may share an underlying defect. This “unified field theory” raises questions about whether defects favoring progressive weight gain and metabolic impairment also contribute to ?-cell decompensation. One potential link could be sustained cell exposure to nutrient concentrations exceeding energy requirements. Deleterious cellular effects of nutrient excess can include impaired inflammatory signaling, endoplasmic reticulum stress, excess production of reactive oxygen species, mitochondrial dysfunction, accumulation of triglycerides and/or fatty acyl intermediates, and activation of serine-threonine kinases. These responses are not mutually exclusive, and induction of one may trigger another, leading to a cascade of damage. Obesity-associated cellular injury can in turn recruit and activate macrophages and other immune cells that exacerbate tissue inflammation. Collectively, these responses contribute to the pathogenesis of insulin resistance in the liver, skeletal muscle, and adipose tissue, and some (e.g., acquired mitochondrial dysfunction and inflammation may occur in ?-cells as well via mechanisms discussed above. Obesity and diabetes have long menaced the population of the entire world. These conditions have now become a global burden. More than 65% people die from heart disease or stroke. Adapting a healthy lifestyle, spreading awareness , getting regular check ups, paying attention to what our body signals and following a proper medicine regime are the only ways of ensuring longer life span. Reducing the burden of obesity and diabetes is solely dependant on partnerships between people and health workers.


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