Autonomic activity and glycemic homeostasis are maintained by precocious and low intensity training exercises in MSG-programmed obese mice.
Current research employed electrical records from superior vagus and sympathetic nerve branch that supply fat retroperitoneal tissue (RS nerve) to investigate whether very moderate swim training in obese-programmed mice would change sympathetic and parasympathetic autonomic nervous system activities. Neonatal mice were treated with monosodium L: -glutamate (MSG), during their first 5 days of life, to induce obesity. Mice started training on weaning, comprising free swimming 3 days/week, 15 min/day for 10 weeks. After 12 h fasting, the nerve electrical signals of the 90-day-old mice were processed to obtain firing rates. Blood samples were collected to measure glucose and insulin levels. Adrenal catecholamine content was measured. MSG treatment caused obesity. Hyperglycemia and hyperinsulinemia in MSG-obese mice, without any change in food intake, were obtained. Vagus firing rates were higher in obese mice than those in lean ones. A decrease in RS nerve activity and lower adrenal catecholamine stores have been observed. Swimming normalized blood glucose and insulin levels and MSG-obesity onset was attenuated by exercise. Vagus activity from obese mice decreased, whereas RS nerve activity and adrenal catecholamine levels increased in trained ones. Results suggest that autonomic activity imbalance and metabolic dysfunctions observed in MSG-obese mice were inhibited by precocious and moderate exercise training.
Scomparin
Dionizia Xavier
DX
Laboratory of Secretion Cell Biology, Department of Cell Biology and Genetics, State University of Maringá, Avenida Colombo 5790, Bloco H-67, S/019, Maringá, PR 87020-900, Brazil.
Gomes
Rodrigo Mello
RM
Grassiolli
Sabrina
S
Rinaldi
Wilson
W
Martins
Adriana Gallego
AG
de Oliveira
Júlio Cezar
JC
Gravena
Clarice
C
de Freitas Mathias
Paulo Cezar
PC
D000313:Adrenal Medulla / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D001341:Autonomic Nervous System / Q000187:drug effects / Q000502:physiology*; D002395:Catecholamines / Q000378:metabolism; D004435:Eating / Q000187:drug effects / Q000502:physiology; D005260:Female; D005947:Glucose / Q000378:metabolism*; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology; D007328:Insulin / Q000378:metabolism; D008297:Male; D051379:Mice; D008820:Mice, Obese; D009765:Obesity / Q000139:chemically induced* / Q000378:metabolism / Q000503:physiopathology*; D010805:Physical Conditioning, Animal / Q000379:methods / Q000502:physiology*; D012970:Sodium Glutamate; D013550:Swimming / Q000502:physiology
D002395:Catecholamines; D007328:Insulin; D005947:Glucose; D012970:Sodium Glutamate