XXXX , metabolism, and @entity101 .

@entity101 @entity28 @entity2690 @entity1735 @entity1372 @entity3190 @entity413
The relationship between @entity28 and @entity101 is complex and poorly understood. A developing body of information suggests that metabolic factors related to the @entity28 state are importantly involved. The pertinent observations include: (1) Diet influences sympathetic nervous system activity. Fasting suppresses, while @entity1735 and fat feeding stimulate, sympathetic activity. (2) Dietary-induced changes in sympathetic activity contribute to the changes in metabolic rate that accompany changes in dietary intake. (3) @entity2690 -mediated @entity413 metabolism in the hypothalamus provides a link between dietary intake and sympathetic nervous system activity. And (4) @entity3190 , a consequence of @entity2690 resistance in the @entity28 , is associated with @entity101 . These observations have suggested the following hypothesis. @entity3190 results in sympathetic stimulation which drives thermogenic mechanisms, thereby increasing metabolic rate. The net result is a restoration of energy balance at the expense of @entity3190 and increased sympathetic activity. @entity101 is thus the unfortunate consequence of @entity3190 , which increases renal @entity1372 reabsorption, and sympathetic stimulation of the heart, kidney, and vasculature. The data on which this hypothesis is constructed are reviewed and the implications discussed.
