HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Accepted manuscript (PDF) All Versions of this Article: JOE-08-0312v1 201/3/351    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Andreazzi, A. E. Articles by Mathias, P.-C. d. F. Search for Related Content PubMed PubMed Citation Articles by Andreazzi, A. E. Articles by Mathias, P.-C. d. F.

A Andreazzi, Cell Biology and Genetics, State University of Maringa, Maringa, Brazil
D Scomparin, Cell Biology and Genetics, State University of Maringa, Maringa, Brazil
F Mesquita, Cell Biology and Genetics, State University of Maringa, Maringa, Brazil
S Balbo, Physiology, State University of Western Parana, Cascavel, Brazil
C Gravena, Cell Biology and Genetics, State University of Maringa, Maringa, Brazil
J De Oliveira, Cell Biology and Genetics, State University of Maringa, Maringa, Brazil
W Rinaldi, Cell Biology and Genetics, State University of Maringa, Maringa, Brazil
R Garcia, Biology, Federal Uniersity of Juiz de Fora, Juiz de Fora, Brazil
S Grassiolli, Cell Biology and Genetics, State University of Maringa, Maringa, Brazil
P Mathias, Cell Biology and Genetics, State University of Maringa, Maringa, Brazil

Correspondence: Paulo-Cezar de Freitas Mathias, Email: pmathias{at}uem.br

Abstract

Swimming exercises by weaning pups inhibited hypothalamic obesity onset and recovered sympathoadrenal axis activity, but this was not observed when exercise training is applied to young adult mice. However, the mechanisms producing this improved metabolism are still not fully understood. Low intensity swimming training started at an early age was undertaken to observe glycemic control in hypothalamic-obese mice produced by neonatal treatment with monosodium L-glutamate (MSG). Whereas MSG and control mice swam for 15 min/day, 3 days a week, from the weaning stage up to 90 days old, sedentary MSG and normal mice did not exercise at all. After 14 h of fasting, animals were killed at 90 days of age. Perigonadal fat accumulation was measured to estimate obesity. Fasting blood glucose and insulin concentrations were also measured. Fresh isolated pancreatic islets were used to test the glucose-induced insulin release and total catecholamine from the adrenal glands was measured. Mice were also submitted to ipGTT. MSG-obese mice showed fasting hyperglycemia, hyperinsulinemia and glucose intolerance. Severe reduction of adrenal catecholamines content has also been reported. Besides the inhibition of fat tissue accretion, exercise caused normalization of insulin blood levels and glycemic control. The pancreatic islets of obese mice, with impaired glucose-induced insulin secretion, were recovered after swimming exercises. Adrenal catecholamine content was increased by swimming. Results show that attenuation of MSG-hypothalamic obesity onset is caused, at least in part, by modulation of sympathoadrenal axis activity imposed by early exercise, which may be associated with subsequent glucose metabolism improvement.