Failure to demonstrate that accelerated gastric emptying after VMH lesions is secondary to excess weight gain

Duggan, J P and Booth, D A (1991) Failure to demonstrate that accelerated gastric emptying after VMH lesions is secondary to excess weight gain. American Journal of Physiology (Regulatory, Integrative and Comparative Physiology), 261 (2). R515-R516. ISSN 0002-9513

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Abstract

BLACK, RICHARD M., KENT L. CONOVER, AND HARVEY P. WEINGARTEN. Accelerated gastric emptying in VMH-lesioned rats is secondary to excess weight gain. Am. J. Physiol. 259 (Regulatory Integrative Comp. Physiol 28): R658-R661, 1990.-This experiment evaluates the hypothesis that an accelerated rate of gastric emptying accounts for the hyperphagia and obesity after lesions of the ventromedial hypothalamus (VMH). Gastric emptying was measured for 16 days after the production of VMH lesions in rats maintained either ad libitum or on restricted eating. Only ad libitum VMH-lesioned rats demonstrated faster than normal rates of emptying. However, VMH rats maintained at control weights showed normal rates of gastric emptying and, even in ad libitum rats, accelerated emptying was not apparent immediately after lesions. These findings indicate that changes of emptying are not a primary effect of VMH lesions but that this dysfunction develops secondarily as a consequence of excess eating and weight gain.
Measurement of stomach secretions demonstrated, however, that VMH lesions did result in an immediate and direct effect on gastric secretion. These findings mitigate the importance of gastric emptying in the etiology of the VMH syndrome. Other data consistent with this conclusion are reviewed.

Item Type: Article
Schools and Departments: School of Psychology > Psychology
Subjects: Q Science > QP Physiology
Q Science > QP Physiology > QP0351 Neurophysiology and neuropsychology
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Depositing User: prof. David Booth
Date Deposited: 28 Aug 2015 11:33
Last Modified: 28 Aug 2015 11:33
URI: http://sro.sussex.ac.uk/id/eprint/56309
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