ON THE MECHANISM OF THE ANOREXIGENIC EFFECT OF ADRENALINE AND AMPHETAMINE

Resumen

Intraperitoneal (i.p.) adrenaline (A) elicited: a strong anorexia and a substantial reduction in spontaneous motor activity which increased wilh the dose; a mild increase or no effect in oxygen consumption (QO₂); negligible changes in rectal temperature (RT); a marked hyperglycemia; and a significant reduction in liver glycogen (LG) that could easily account for the hyperglycemia quantitatively. On the other hand, the isoanorexigenic close of amphetamine (Am) elicited: a great increase in erratic spontaneous activity; a large increase in QO₂ and RT,
no hyperglycemia, but a similar decrease in LG. Therefore, both substances caused the same increase in the rate of glucose liberation by the liver, but in the case of Am, the glucose was consumed by the marked motor activity, resulting in little hyperglycemia. Nevertheless, if the hepatic glucoreceptors are sensitive to the rate of glucose transport through the cell membrane, they could be the main cause of the anorexia produced by both A and Am. The hypothetical sequence of events would be, for A: a primary glycogenolytic effect causing satiation, which in turn causes decrease in activity; this masks or even reverses the primary calorigenic effects of A. No activation of the central nervous system (CNS) is produced, because most A is destroyed in the liver and the small amount that reaches the general circulation does not traverse the bloodbrain barrier (BBB). In the case
of Am: there would be no primary glycogenolytic effects. Most of the substance would reach the general circulation, and would easily traverse the BBB, stimulate the CNS and produce the increase in activity, with a concomitant increase in sympathetic activity that causes an hepatic glycogenolysis. This latter is monitored
by the hepatic glucoreceptors and produces anorexia. That the increase in activity is related to the other changes is shown by the lack of effect, of Am on QO₂ and RT in anesthetized animals.