Abstract
Evidence has accumulated over the past 2 decades to show that the regulation of the fat body mass is integrated in the control of food intake. It was suggested long ago that the metabolic stimulation to eat originated from a shortage of available circulating metabolites; particularly, glucose uptake and utilization has been a central feature of many hypotheses since Mayer's glucostatic theory. In the first section of this contribution, evidence is presented that in rats and man a premeal decline in blood glucose concentration is causally related to meal initiation. The origin of the decline and the possible role of "glycemia-sensitive" neurons located in the lateral hypothalamus (LH) as central sensors of this metabolic stimulus to eat are discussed. In the second section, it is suggested that LH energy utilization and ventro-medial hypothalamus (VMH) energy storage reflect metabolic change at the periphery and also determined the neuronal activity which monitors storage or mobilization of fuels into and from stores. Since glucose is a precursor of triglycerides deposited in adipose tissue and since oxidation of fatty acids in peripheral tissues has a glucose-sparing effect, circulating glucose seems a likely candidate for the signal mediating the effect of fat deposits on food intake.
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