akb48二期生:翻译(有分吆,翻译的好还加分呢???!!我有的是分)

Although such monogenic obesity syndromes are rare (see review by Barsh et al., pp. 644–651), the successful use of murine models to study human obesity indicates that substantial homology exists across mammalian species in the functional organization of the weightregulatory system. More importantly, the identification of molecules that control food intake has generated new targets for drug development in the treatment of obesity and related disorders. Optimism that we may soon enter an era of improved obesity treatment, therefore, seems justified.
Because of the enormous toll on human health taken byobesityandrelateddisorders,animprovedunderstandingof the control of food intake is an important priority. However, the growing number of molecules implicated in energy homeostasis raises nearly limitless possibilities for how body-weight regulation might occur. The aim of this article is to review these advances and to present them in the context of a model for long-termmaintenanceofenergy homeostasis.
Model for energy homeostasis
The increase of food intake (hyperphagia) triggered by a period of fasting is a simple but compelling example of foodintake regulation. The consequent recovery of lost body weight to baseline values, accompanied by the gradual return to normal levels of energy intake6, is testimony to a regulatory process that is both precise and robust. To explain this phenomenon, Kennedy proposed7 in 1953 that inhibitory signals generated in proportion to body fat stores act in the brain to reduce food intake. Thus, when weight loss induced by caloric restriction reduces the level of these inhibitory signals, food intake increases until the energy deficit is corrected. This model, however, does not explain how energy intake is controlled during individual meals. Twenty years later, Gibbs and Smith proposed8 that signals generated during a meal (termed ‘satiety factors’), including peptides secreted from the gastrointestinal tract, provide information to the brain that inhibits feeding and leads to meal termination. A modelthat seems to unite schematically in Fig. 1.