Pathophysiology and aetiology of obesity
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- 作者：John P.H. Wilding
- 关键词：appetite ; genetics ; ghrelin ; hypothalamus ; leptin ; metabolic rate ; obesity ; Prader– ; Willi syndrome ; pro-opiomelanocortin ; satiety
- 刊名：Medicine
- 出版年：2011
- 出版时间：January 2011
- 年：2011
- 卷：39
- 期：1
- 页码：6-10
- 全文大小：161 K
文摘
The epidemic of obesity is already having major effects on population health. Obesity develops in an individual when energy intake exceeds energy expenditure over a long period. The biological processes regulating energy balance are very tightly regulated. However, these mechanisms of appetite control can easily be overwhelmed by a willingness to eat when not hungry if attractive food is provided in inductive settings. Control pathways include short-term signalling of hunger and satiety with hormones derived from the gastrointestinal tract to the central nervous system, long-term signalling of energy stores via leptin and insulin to the brain, and control of metabolism. Rare genetic syndromes that present in early childhood with severe obesity (such as leptin deficiency and mutations in the pro-opiomelanocortin gene) demonstrate that these pathways are biologically important in humans. Most obesity develops as a result of modern lifestyles in genetically susceptible individuals. These changes include increased consumption of high-energy food at the same time as physical activity levels have declined dramatically; in many societies less affluent people seem to be most at risk. Other causes of obesity that should be considered include drugs that increase appetite and structural damage to areas of the central nervous system involved in appetite control, such as the hypothalamus.