Obesity and thinness: insights from genetics

被引:4
作者
Farooqi, Sadaf [1 ]
机构
[1] Addenbrookes Hosp, Wellcome MRC Inst Metab Sci, Box 289, Cambridge CB2 0QQ, England
关键词
genetics; obesity; thinness; leptin; melanocortin; hyperphagia; EARLY-ONSET OBESITY; BODY-MASS INDEX; MC4R AGONIST; LEPTIN; DEFICIENCY; MUTATIONS; SETMELANOTIDE; NEURONS; TWINS;
D O I
10.1098/rstb.2022.0205
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Genetic disruption of key molecular components of the hypothalamic leptin-melanocortin pathway causes severe obesity in mice and humans. Physiological studies in people who carry these mutations have shown that the adipose tissue-derived hormone leptin primarily acts to defend against starvation. A lack of leptin causes an intense drive to eat and increases the rewarding properties of food, demonstrating that human appetite has a strong biological basis. Genetic studies in clinical- and population-based cohorts of people with obesity or thinness continue to provide new insights into the physiological mechanisms involved in weight regulation and identify molecular targets for weight loss therapy.This article is part of a discussion meeting issue 'Causes of obesity: theories, conjectures and evidence (Part II)'.
引用
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页数:4
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