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Elsevier Science

Physiol Behav. 1989 Jun;45(6):1123-9. doi: 10.1016/0031-9384(89)90098-x.

The effects of adrenalectomy, corticotropin releasing factor and vasopressin on the sympathetic firing rate of nerves to interscapular brown adipose tissue in the Zucker rat.

Physiology & behavior

S J Holt, D A York

Affiliations

  1. Department of Human Nutrition, School of Biological and Physiological Sciences, Southampton University, England.

PMID: 2554347 DOI: 10.1016/0031-9384(89)90098-x

Abstract

The firing rate of the sympathetic efferent nerves to interscapular brown adipose tissue (IBAT) is lower in the obese rat compared with the lean rat. The present experiments show that adrenalectomy has no effect on nerve firing rate in the lean rat and a small but statistically nonsignificant effect in the obese rat. Injection of corticotropin releasing factor (CRF) into the IIIrd ventricle produced a dose dependent increase in the firing rate of the sympathetic nerves to interscapular brown adipose tissue (IBAT) in both lean and obese rats. The basal (unstimulated) level of firing was lower in the obese rat compared with the lean rat and remained significantly below lean values at each dose. The minimum dose of CRF to see an effect (125 ng) and the dose at which maximum effect on nerve firing rate was observed (500 ng) was similar in both genotypes. Injection of adrenocorticotropic hormone (ACTH) had no effect on nerve firing rate to IBAT. Central administration of vasopressin produced a significant increase in sympathetic firing rate to IBAT in both lean and obese rats. The temperature of IBAT was also significantly increased with vasopressin and the duration of the response was longer compared with CRF, but the minimum dose to see an effect was higher (2.5 micrograms). The response to vasopressin was greater in the obese rat compared with the lean rat but the maximum firing rate did not achieve levels observed in lean rats. Chronic infusion of CRF into the IIIrd ventricle of obese rats resulted in a reduction of food intake and body weight gain but IBAT mitochondrial GDP binding was unaltered by the treatment. These data are consistent with the hypothesis that the defect in the obese Zucker rat may be due to a glucocorticoid inhibition of CRF and/or vasopressin action in the CNS.

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