Systemic phlorizin prevents gold thioglucose necrosis in the ventromedial hypothalamus

Intraventricular and intrahypothalamic infusions of phlorizin (PHL) are known to cause hyperphagia and to prevent gold thioglucose (GTG) lesion formation in the ventromedial hypothalamus (VMH), respectively. In this study, PHL, administered IP in a large dose (900 mg/kg), completely inhibited GTG ne...

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Bibliographic Details
Published inBrain research bulletin Vol. 8; no. 4; p. 347
Main Authors Brown, D F, Viles, J M
Format Journal Article
LanguageEnglish
Published United States 01.04.1982
Subjects
Animals
Aurothioglucose - toxicity
Female
Gold - toxicity
Hypothalamus - drug effects
Hypothalamus - pathology
Median Eminence - physiology
Mice
Necrosis
Phlorhizin - pharmacology
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Summary:Intraventricular and intrahypothalamic infusions of phlorizin (PHL) are known to cause hyperphagia and to prevent gold thioglucose (GTG) lesion formation in the ventromedial hypothalamus (VMH), respectively. In this study, PHL, administered IP in a large dose (900 mg/kg), completely inhibited GTG necrosis in the VMH. PHL did not cause excessive urinary excretion of GTG. This evidence suggested that 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 less than 0.001). Small amounts of PHL elevated VMH glucose oxidation (p less than 0.001). Since PHL is an inhibitor of glucose transport, these data support the concept of a hypothalamic glucostatic modulation for the control of food intake.
ISSN:0361-9230
DOI:10.1016/0361-9230(82)90071-5