title: Absence of altered autophagy after myocardial ischemia in diabetic compared with nondiabetic mice.
abstract: OBJECTIVE
  The extent of autophagy in myocardium following persistent ischemia and the effects of insulin resistance and diabetes on cardiac autophagy following myocardial infarction (MI) have not been well elucidated. It is generally thought that autophagy reflects the nutritional status of cells, presumably alterable by diabetes. It has been conjectured that diminution of autophagy early after the onset of MI may preserve jeopardized myocardium thereby improving prognosis.
  
  
  METHODS
  Ten-week-old nondiabetic C57BL6 mice, 20-week-old diabetic and nondiabetic C57BL6 mice were subjected to MI for 4 weeks. Hearts from these mice were harvested and assayed for markers of autophagy.
  
  
  RESULTS
  Hearts of 10-week-old C57BL6 mice subjected to 4 weeks of MI had similar levels of LC3-II, a protein indicator of autophagy, as measured by western blotting compared with hearts from sham operated controls. In 20-week-old C57BL6 mice rendered diabetic by feeding a high-fat diet, the amounts of autophagy were comparable to those in 20-week-old nondiabetic C57BL6 mice on a normal diet.
  
  
  CONCLUSIONS
  The magnitude of autophagy in the heart after infarction is of very modest extent and is not modulated by diabetes. Thus, diminution of autophagy is not likely to reduce infarct size or attenuate late negative remodeling after MI in patients with diabetes.
authors.affiliation: Cardiovascular Research Institute, University of Vermont College of Medicine, Vermont 05466, USA.
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: French
authors.forename: Akm
authors.initials: A
authors.lastname: Tarikuz Zaman
authors.forename: Keara L
authors.initials: KL
authors.lastname: McElroy-Yaggy
authors.forename: Dagnija K
authors.initials: DK
authors.lastname: Neimane
authors.forename: Burton E
authors.initials: BE
authors.lastname: Sobel
mesh_terms: D000818:Animals; D001343:Autophagy; D015415:Biomarkers / Q000378:metabolism; D015153:Blotting, Western; D048909:Diabetes Complications / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D003921:Diabetes Mellitus, Experimental / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D005951:Glucose Tolerance Test; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D009203:Myocardial Infarction / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D017202:Myocardial Ischemia / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D010766:Phosphorylation; D038601:Ribosomal Protein S6 / Q000378:metabolism; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism; D013997:Time Factors
chemical_list: D015415:Biomarkers; C480860:Map1lc3b protein, mouse; D008869:Microtubule-Associated Proteins; D038601:Ribosomal Protein S6; C546843:mTOR protein, mouse; D058570:TOR Serine-Threonine Kinases