文摘
The sympathetic nervous system (SNS) has an essential role in the maintenance of metabolic, gastrointestinal and cardiovascular homeostasis. Activation of SNS involves noradrenaline release by noradrenergic fibers and adrenaline secretion by adrenal medulla. The SNS has a major role in the control of adipose tissue function both directly, on adipocytes and adipose tissue vessels, and due to effects on pancreatic hormones secretion. Although a number of previous findings on SNS activity evaluation in humans provided inconsistent findings, various alterations of SNS effects on metabolism have been now implicated in the development and the maintenance of obesity. SNS activity to the skeletal muscle, evaluated via muscle sympathetic nerve activity (MSNA), is related to early renal, cardiac and endothelial dysfunctions in the obese. Reduced SNS activity has been claimed to represent a risk factor for weight gain. However, elevated SNS activity is present in obesity. Increased baseline SNS activity and blunted SNS-mediated thermogenic response to a meal may play a role in the progression of obesity related metabolic and cardiovascular diseases. Alterations of fat cell adrenergic receptor-mediated responses have been reported in the obese; they suggest an adaptation of adipose tissue to the level of SNS activity. This review provides an overview of physiological aspects of the SNS involvement in normal and obese subjects. Physiological and pathological changes in SNS activity are summarized. Modifications occurring in adipose tissue function and fat cell responsiveness to noradrenaline and adrenaline are also considered.