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The Molecular Basis of Body Weight Control

机译:体重控制的分子基础

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摘要

Obesity is defined as a condition of excess body weight due to an increased amount of energy accumulated in the form of fat in adipose tissue depots. It can occur as a result of genetic or acquired changes in different types of biochemical processes leading, to an amount of energy intake that, in the long term, exceeds energy expenditure. Obesity and even a moderate overweight are viewed as pathological conditions when the excess and/or the type of excess fat are able to produce adverse health consequences. The rising incidence of obesity in developed Western countries is not conceivable as a consequence of a sudden genomic change but as a consequence of environmental changes. We do not know what are the precise environmental factors involved except that they are associated with the availability and composition of food in our rich societies and with the trend to less physical activity due to new life style habits and social requirements. Our organisms appear to be better adapted to avoid weight loss than to combat weight gain, probably because for many years our species has evolved under conditions of limited food supply. However, it is of note that the response to diet and the predisposi- tion to overweight gain varies widely between individuals, reflecting genetic and biochemical individuality of the body weight control mechanisms. Obesity represents the archetype of phenotypic complexity: very diverse processes or factors that affect the size and composition of any tissue, organ or individual system in our organism can affect body weight. However, only those factors that affect overall energy balance in the long term, and, consequently the amount of fat reserves, can be considered as part of the body weight control system. The present article is aimed to a conceptual description of these processes, their mechanisms and their interrelationships. Taken together, these processes define a coherent physiological system for the regulation of body fat reserves and body weight. In Figure 1 this system is schematically represented, highlighting the role of leptin in this complex regulatory net.
机译:肥胖被定义为由于脂肪组织贮库中以脂肪形式积累的能量增加而导致体重过重的状况。它可能是由于不同类型的生化过程中的遗传或获得性变化而导致的,从长远来看,导致的能量摄入量超过了能量消耗。当过量和/或过量脂肪的类型能够对健康产生不利影响时,肥胖症甚至中等程度的超重就被视为病理状况。在西方发达国家,肥胖的发生率上升并不是由于基因组突变而引起的,而是由于环境变化而引起的。我们不知道确切的环境因素是什么,除了它们与我们丰富的社会中食物的可获得性和组成以及与新的生活方式和社会要求引起的体育锻炼减少的趋势有关。我们的生物似乎比避免体重增加更能避免体重减轻,这可能是因为我们的物种已经在有限的食物供应条件下进化了许多年。然而,值得注意的是,饮食对饮食的反应以及对超重增加的诱因在个体之间差异很大,这反映了体重控制机制的遗传和生化特征。肥胖代表着表型复杂性的原型:影响我们机体中任何组织,器官或单个系统的大小和组成的非常多种多样的过程或因素都可以影响体重。但是,只有那些会长期影响总体能量平衡并进而影响脂肪储备量的因素才能被视为体重控制系统的一部分。本文旨在对这些过程,其机制及其相互关系进行概念上的描述。综上所述,这些过程定义了用于调节体内脂肪储备和体重的连贯的生理系统。在图1中,该系统被示意性地表示,突出了瘦蛋白在这个复杂的调节网络中的作用。

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