Level of satiety: fatty acid and glucose metabolism in three brain sites associated with feeding.

Two experiments were conducted to determine if the level of satiety alters fatty acid and glucose metabolism in selected brain areas. Rats received 150, 100, or 50% of normal intake by gastric intubation for 7 days. Thus the impetus for spontaneous feeding would be impaired in 150% fed rats (anoretic), potentiated in 50% fed rats (hungry), and maintained in 100% fed (control) rats. In vitro metabolism of glucose and palmitate was examined in liver, cortex, ventrolateral hypothalamus (VLH), ventromedial hypothalamus (VMH), and area postrema nucleus of the solitary tract. The VLH of hungry (50%) rats had a 40% increase in palmitate oxidation and a 9% decrease in glucose oxidation compared with controls (100%). The VLH of anoretic rats (150%) had a 36% decrease in palmitate oxidation and a 20% increase in glucose oxidation compared with controls. Hepatic metabolic differences were similar to those seen in VLH. Total fatty acid synthesis was 37% higher in anoretic and 29% lower in hungry compared with control rats. Recognition of excess, sufficient, or deficient peripheral energy status may be a process that monitors both VLH energy utilization and VMH energy storage in an attempt to depict metabolic adaptations of the periphery.