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Obesity background
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== Pathophysiology == * In general, there is persistent hunger that is not satiated by the amounts of food that satisfy the non-obese ** This leads to long-term positive energy balance, and accumulation of adipose tissue ** Adipose tissue eventually develops reduced ability to assimilate excess calories ** This leads to fat redistribution to other tissues, causing diverse health consequences * Metabolic actions of adipose tissue ** Increased secretion of 'adipokines' - leptin, adiponectin, resistin and inflammatory cytokines - comes from white fat, as opposed to brown fat ** Causes chronic low-grade inflammation, interfering with cellular processes, leading to metabolic derangements (T2DM, etc) * Ghrelin - the 'hunger hormone' ** Levels decrease after meals ** Acts on hypothalamus ** Primarily produced in fundus of stomach ** Regulates hunger together with leptin * Genetic ** Specific genes - FTO, MC4R - however these only rarely are the sole cause of obesity, and generally become apparent in childhood. ** Syndromes - Prader-Willi (deficits in ghrelin signalling) * Microbiome ** May be a relationship between gut microbiome and obesity, suggested by some animal studies * Nutrition ** Hypoalbuminaemia ** Vitamin and micronutrient deficiencies are common * Weight regain ** Body defends fat vigorously ** Increased hunger, driven by ghrelin ** Decreased energy expenditure, driven by multifactorial neurohormonal changes including reduced SNS input
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