title: Exercise training attenuates cerebral ischemic hyperglycemia by improving hepatic insulin signaling and β-cell survival.
abstract: OBJECTIVE
  Preventing hyperglycemia after acute stroke attenuates complications of cerebral ischemia and reduces the risk of mortality. We investigated whether regular exercise prevents neuronal cell death and post-stroke hyperglycemia in gerbils after cerebral ischemia.
  
  
  METHODS
  Cerebral ischemia was induced by carotid artery occlusion for 8min. The gerbils that underwent ischemic or sham operations were randomly subdivided into exercise (ran on inclined treadmill at 20m/min for 30min 5days per week for 1week prior to surgery) or non-exercise groups. Gerbils were fed a 40% fat diet and after 28days, glucose metabolism, serum cytokine levels and cognitive function was measured.
  
  
  RESULTS
  Artery occlusion resulted in a 64% reduction in hippocampal CA1 neurons in comparison to the sham gerbils, and caused decreased neuronal mass and impaired cognitive function. Exercise partially prevented neuronal death and improved ischemia-induced glucose intolerance. Ischemia decreased hepatic insulin signaling and exacerbated insulin resistance whereas exercise prevented the disturbance. Insulin secretion was lower in ischemic gerbils than sham gerbils, due to lowered pancreatic β-cell mass caused by increased β-cell apoptosis and decreased β-cell proliferation, which were also prevented by exercise. Increase of apoptosis was associated with elevated caspase-3 activity, consistent with increased serum tumor necrosis factor (TNF)-α and interleukin (IL)-1β levels.
  
  
  CONCLUSIONS
  Hippocampal neuronal cell death induces hyperglycemia due to attenuated hepatic insulin signaling and decreased β-cell mass by increased β-cell apoptosis through increased TNF-α and IL-1β levels. Exercise partially prevents this phenomenon suggesting that exercise training may provide neuroprotective benefits from cerebral ischemic hyperglycemia.
authors.affiliation: Dept. of Food & Nutrition, College of Natural Science, Obesity/Diabetes Research Institutes, Hoseo University, Asan-Si, South Korea. smpark@hoseo.edu
authors.forename: Sunmin
authors.initials: S
authors.lastname: Park
authors.forename: Da Sol
authors.initials: DS
authors.lastname: Kim
authors.forename: Sunna
authors.initials: S
authors.lastname: Kang
mesh_terms: D000818:Animals; D017209:Apoptosis; D002545:Brain Ischemia / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D056547:CA1 Region, Hippocampal / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D002470:Cell Survival; D003071:Cognition; D005849:Gerbillinae; D006943:Hyperglycemia / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D007328:Insulin / Q000378:metabolism*; D050417:Insulin-Secreting Cells / Q000378:metabolism* / Q000473:pathology; D053583:Interleukin-1beta / Q000378:metabolism; D008099:Liver / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D010805:Physical Conditioning, Animal; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D007328:Insulin; D053583:Interleukin-1beta; D014409:Tumor Necrosis Factor-alpha
keywords: Apoptosis; Cerebral ischemia; Glucose; Insulin; β-cell