移民了还能恢复国籍吗:求助翻译高手!!(专业论文翻译)急!急!急!急!

Central nervous system control of food intake
New information regarding neuronal circuits that control food intake and their hormonal regulation has extended our understanding of energy homeostasis, the process whereby energy intake is matched to energy expenditure over time. The profound obesity that results in rodents (and in the rare human case as well) from mutation of key signalling molecules involved in this regulatory system highlights its importance to human health. Although each new signalling pathway discovered in the hypothalamus is a potential target for drug development in the treatment of obesity, the growing number of such signalling molecules indicates that food intake is controlled by a highly complex process. To better understand how energy homeostasis can be achieved, we describe a model that delineates the roles of individual hormonal and neuropeptide signalling pathways in the control of food intake and the means by which obesity can arise from inherited or acquired defects in their function.

For most of us, the composition and amount of food that we eat varies considerably from one meal to the next and from one day to the next. Our common experience, therefore, seems at odds with the hypothesis that food intake is highly regulated. Emotions, social factors, time of day, convenience and cost are but a few of the variables that are not biologically regulated, but nonetheless affect meal-to-meal energy intake. As a consequence, daily energy intake is variable both within and among individuals, and is not well correlated with daily energy expenditure1. Despite short-term mismatches in energy balance, however, most of us match cumulative energy intake to energy expenditure with great precision when measured over a period that spans many meals1. This phenomenon reflects an active regulatory process, termed energy homeostasis, that promotes stability in the amount of body energy stored in the form of fat. Although it is overly simplistic to reduce a behaviour as complex as feeding to a series of molecular interactions, discoveries over the past few years have identified signalling molecules that affect food intake and that are critical for normal energy homeostasis. The application of molecular genetics to mice has been especially important in this effort. For example, several monogenic forms of human obesity were identified by searching for mutations homologous to those causing obesity in mice2–5.