Adrenaline anorexia blocked by alpha and beta adrenergic antagonists in 24-h fasted rats.

The effect of alpha and beta adrenergic blockers, phentolamine (PH) and propranolol (PR), on the anorexia induced by intraperitoneal (i.p.) adrenaline (A) was studied in 24 h-fasting male and female adult Wistar rats. I.p. PH elicited a small but significant increase in food intake in both males and females. The combination of PH + PR completely blocked the anorexia elicited by i.p. A in both males and females. In females, PH and PR alone partially blocked A-induced anorexia. In males, PH had no significant effect on A-induced anorexia but PR blocked it completely. It was concluded that the relative participation of alpha and beta adrenergic receptors in A-induced anorexia seems to depend on the sex of the rat, at least for the doses used in the present study: in females, alpha and beta actions seem to be approximately equal, while in males the beta is predominant.

Glycogenolytic substances, hepatic and systemic lactate, and food intake in rats.

Changes in hepatic lactate and glucose and systemic blood lactate produced by intraperitoneal injections of epinephrine, isoproterenol, glucagon, and insulin showed a high correlation (r = 0.9) with the changes in food intake elicited by the same substances. The changes in systemic blood glucose showed no correlation with the changes in feeding, which suggests that central glucoreceptors are not playing an important role in the observed changes in feeding. The intramuscular epinephrine had no significant effect on food intake, in spite of changes in systemic and hepatic lactate and glucose similar to those elicited by intraperitoneal epinephrine. However, intramuscular epinephrine had no hepatic glycogenolytic effect. This suggests that the changes in glucose and lactate elicited by intraperitoneal epinephrine result from hepatic glycogenolysis, whereas the changes elicited by intramuscular epinephrine result from muscular glycogenolysis and inhibition of insulin. Thus hepatic glucose and lactate are good predictors of feeding only when they are produced endogenously by hepatic glycogenolysis. It was concluded that hepatic lactate cannot be the substance sensed by hepatic metabolic receptors. However, due to a possible change in the hepatic lactate-to-pyruvate ratio elicited by intraperitoneal epinephrine, hepatic pyruvate may still be correlated with feeding during the action of both intramuscular and intraperitoneal epinephrine. Therefore the hypothesis that pyruvate is the substance monitored by hepatic metabolic receptors should be tested.