Abstract Title:

Low-Intensity swimming training after weaning improves glucose and lipid homeostasis in MSG hypothalamic obese mice.

Abstract Source:

Biomed Sci Instrum. 2007;43:272-7. PMID: 21539446

Abstract Author(s):

Dionízia Xavier Scomparin, Sabrina Grassiolli, Rodrigo Mello Gomes, Rosana Torrezan, Júlio Cezar de Oliveira, Clarice Gravena, Carolina Costa Pêra, Paulo Cezar de Freitas Mathias

Article Affiliation:

Laboratory of Secretion Cell Biology, Department of Cell Biology and Genetics, State University of Maringá, Maringá, Paraná, Brazil.


Low-intensity swimming training, started at an early age, was undertaken to observe glycemic control in hypothalamic obese mice produced by neonatal monosodium l-glutamate (MSG) treatment. Although swimming exercises by weaning pups inhibited hypothalamic obesity onset and recovered sympathoadrenal axis activity, this event was not observed when exercise training is applied to young adult mice. However, the mechanisms producing this improved metabolism are still not fully understood. Current work verifies whether, besides reducing fat tissue accumulation, low-intensity swimming in MSG-weaned mice also improves glycemic control. Although 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. Retroperitonial fat accumulation was measured to estimate obesity. Fasting blood glucose and insulin concentrations were also measured. Mice were also submitted to ipGTT. MSG obese mice showed fasting hyperglycemia, hyperinsulinemia, and glucose intolerance and insulin resistance. However, the exercise was able to block MSG treatment effects. Higher total cholesterol and triglycerides observed in MSG mice were normalized by exercise after weaning. Exercised MSG animals had higher HDLc than the sedentary group. Data suggest that early exercise training maintains normoglycemia, insulin tissue sensitivity, and normal lipid profile in mice programmed to develop metabolic syndrome.

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