SYSTEMIC PHLORIZIN PREVENTS GOLD THIOGLUCOSE NECROSIS IN THE VENTROMEDIAL HYPOTHALAMUS

Intraventricular and intrahypothalamic infusions of phlorizin (PHL) cause hyperphagia and prevent gold thioglucose (GTG) lesion formation in the ventromedial hypothalamus (VMH), respectively. PHL, administered i.p. in a large dose (900 mg/kg), completely inhibited GTG necrosis in the mouse VMH. PHL did not cause excessive urinary excretion of GTG. Systemic PHL must be injected in a high concentration to alter the hypothalamic response to GTG. In vitro measurements of VMH glucose oxidation substantiated this idea. Only at a high concentration of PHL was glucose oxidation significantly depressed in the VMH (P < 0.001). Small amounts of PHL elevated VMH glucose oxidation (P < 0.001). Since PHL is an inhibitor of glucose transport, the data support the concept of a hypothalamic glucostatic modulation for the control of food intake.