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Experimental Diabetes Research
Volume 2011, Article ID 947917, 11 pages
Research Article

Impaired Sympathoadrenal Axis Function Contributes to Enhanced Insulin Secretion in Prediabetic Obese Rats

1Laboratory of Physiology, Department of Physiology, Federal University of Juiz de Fora, 36036-900 Juiz de Fora, MG, Brazil
2Laboratory of Secretion Cell Biology, Department of Cell Biology and Genetics, State University of Maringá, 87020-900 Maringá, PR, Brazil
3Laboratory of Cell Biology, Department of Biology, Federal University of Juiz de Fora, 36036-900 Juiz de Fora, MG, Brazil

Received 14 April 2011; Accepted 13 June 2011

Academic Editor: Stavros Liatis

Copyright © 2011 Ana Eliza Andreazzi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The involvement of sympathoadrenal axis activity in obesity onset was investigated using the experimental model of treating neonatal rats with monosodium L-glutamate. To access general sympathetic nervous system activity, we recorded the firing rates of sympathetic superior cervical ganglion nerves in animals. Catecholamine content and secretion from isolated adrenal medulla were measured. Intravenous glucose tolerance test was performed, and isolated pancreatic islets were stimulated with glucose and adrenergic agonists. The nerve firing rate of obese rats was decreased compared to the rate for lean rats. Basal catecholamine secretion decreased whereas catecholamine secretion induced by carbachol, elevated extracellular potassium, and caffeine in the isolated adrenal medulla were all increased in obese rats compared to control. Both glucose intolerance and hyperinsulinaemia were observed in obese rats. Adrenaline strongly inhibited glucose-induced insulin secretion in obese animals. These findings suggest that low sympathoadrenal activity contributes to impaired glycaemic control in prediabetic obese rats.