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This Article Full Text Full Text (PDF) All Versions of this Article: 288/1/E254    most recent 00087.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (8) Citing Articles via Google Scholar Google Scholar Articles by Duclos, M. Articles by Richard, D. Search for Related Content PubMed PubMed Citation Articles by Duclos, M. Articles by Richard, D.

Corticosterone-dependent metabolic and neuroendocrine abnormalities in obese Zucker rats in relation to feeding

¹Centre de recherche de l'Hôpital Laval et Centre de recherche sur le métabolisme énergétique de l'Université Laval, Quebec, Canada; ²Laboratoire Neurogénétique et Stress, Institut National de la Santé et de la Recherche Médicale U471, Université Bordeaux, Bordeaux, France

Submitted 22 February 2004 ; accepted in final form 9 September 2004

The obese Zucker (fa/fa) rat is characterized by hyperphagia, hyperinsulinemia, an increase in fat deposition, and a hyperactivity in the hypothalamic-pituitary-adrenal (HPA) axis. The HPA axis in fa/fa rats is hypersensitive to stressful experimental conditions. Food deprivation even leads to a stress reaction in obese fa/fa rats. The present study was conducted to investigate the role of corticosterone in obese rats on the basal, fasting, and postprandial metabolic rate as well as on the central expression of the thyrotropin-releasing hormone (TRH) in these conditions. In addition, the study was aimed at clarifying whether the high levels of corticosterone in obese rats are responsible for the induction of the stress reaction to food deprivation in these animals. The present results demonstrate that whole body fat oxidation and postprandial metabolic responses in obese Zucker rats were improved by adrenalectomy (ADX). At the level of the central nervous system, ADX reversed a decrease in TRH mRNA expression in the paraventricular hypothalamus (PVH) detected in fasting animals. Considering all feeding conditions, the obese rats demonstrated lower TRH mRNA levels compared with lean animals. ADX resulted in an enhanced postprandial activation of the parvocellular PVH. In contrast, the magnocellular part of the PVH was less responsive to refeeding in ADX animals. Finally, ADX failed to prevent the stress response of obese rats to food deprivation. The present results provide evidence that the removal of adrenals resolve some of the metabolic defects encountered in obese Zucker rats. They also demonstrate that not all the abnormalities of the obese Zucker rats are attributable to the hyperactivity of the HPA axis.

fa/fa rats; metabolic rate; sympathetic nervous system; food deprivation; refeeding; thyrotropin-releasing hormone; tyrosine hydroxylase; corticotropin-releasing hormone

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