title: Glycolytic and mitochondrial metabolism in pancreatic islets from MSG-treated obese rats subjected to swimming training.
abstract: OBJECTIVE
  Obese rats obtained by neonatal monosodium glutamate (MSG) administration present insulin hypersecretion. The metabolic mechanism by which glucose catabolism is coupled to insulin secretion in the pancreatic β-cells from MSG-treated rats is understood. The purpose of this study was to evaluate glucose metabolism in pancreatic islets from MSG-treated rats subjected to swimming training.
  
  
  METHODS
  MSG-treated and control (CON) rats swam for 30 minutes (3 times/week) over a period of 10 weeks. Pancreatic islets were isolated and incubated with glucose in the presence of glycolytic or mitochondrial inhibitors.
  
  
  RESULTS
  Swimming training attenuated fat pad accumulation, avoiding changes in the plasma levels of lipids, glucose and insulin in MSG-treated rats. Adipocyte and islet hypertrophy observed in MSG-treated rats were attenuated by exercise. Pancreatic islets from MSG-treated obese rats also showed insulin hypersecretion, greater glucose transporter 2 (GLUT2) expression, increased glycolytic flux and reduced mitochondrial complex III activity.
  
  
  CONCLUSIONS
  Swimming training attenuated islet hypertrophy and normalised GLUT2 expression, contributing to a reduction in the glucose responsiveness of pancreatic islets from MSG-treated rats without altering glycolytic flux. However, physical training increased the activity of mitochondrial complex III in pancreatic islets from MSG-treated rats without a subsequent increase in glucose-induced insulin secretion.
authors: Department of General Biology, State University of Ponta Grossa, Ponta Grossa, PR 84030-900, Brazil. naaleite@hotmail.com
authors: Nayara de Carvalho
authors: Nde C
authors: Leite
authors: Thiago Rentz
authors: TR
authors: Ferreira
authors: Sarah
authors: S
authors: Rickli
authors: Patricia Cristine
authors: PC
authors: Borck
authors: Paulo Cezar de Freitas
authors: PC
authors: Mathias
authors: Henriette Rosa de Oliveira
authors: HR
authors: Emilio
authors: Sabrina
authors: S
authors: Grassiolli
mesh_terms: D017667:Adipocytes / Q000473:pathology; D000818:Animals; D004195:Disease Models, Animal; D014450:Electron Transport Complex III / Q000378:metabolism; D005503:Food Additives / Q000494:pharmacology*; D051273:Glucose Transporter Type 2 / Q000378:metabolism; D006019:Glycolysis / Q000187:drug effects; D006984:Hypertrophy / Q000378:metabolism; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism; D009765:Obesity / Q000378:metabolism* / Q000473:pathology; D010805:Physical Conditioning, Animal; D051381:Rats; D017208:Rats, Wistar; D012970:Sodium Glutamate / Q000494:pharmacology*
chemical_list: D005503:Food Additives; D051273:Glucose Transporter Type 2; D007328:Insulin; D014450:Electron Transport Complex III; D012970:Sodium Glutamate