title: Insulin treatment of diabetic rats reduces cardiac function in a lipopolysaccharide-induced systemic inflammation model.
abstract: BACKGROUND
  Diabetes is a common comorbidity in patients with various medical conditions. Tight glucose control is known to improve systemic inflammation; however, whether it is effective in diabetic patients is unknown. The purpose of this study was to examine how strict glucose control affects systemic inflammation in diabetic patients.
  
  
  METHODS
  Male Wistar rats. We determined the effect of insulin therapy on cardiac function in a rat model of systemic inflammation. We administered lipopolysaccharide intravenously, with or without insulin, to streptozotocin-induced diabetic rats. After induction of systemic inflammation, we determined serum cytokine (IL-6 and TNFα) and nitrate/nitrite levels and measured cardiac function.
  
  
  RESULTS
  Cytokine levels and cardiac function were significantly reduced in diabetic rats compared to non-diabetic rats. Moreover, insulin treatment was associated with higher cytokine levels and decreased cardiac function.
  
  
  CONCLUSIONS
  In systemic inflammatory conditions, diabetes increases various proinflammatory mediators and inhibits cardiac function; insulin treatment exacerbates these effects. Thus, strict glucose control may not be desirable in diabetic patients with systemic inflammatory conditions.
authors.affiliation: Department of Anesthesiology and Intensive Care Medicine, Oita University Faculty of Medicine, Yufu City, Oita, Japan. saku@med.oita-u.ac.jp
authors.forename: Satoshi
authors.initials: S
authors.lastname: Hagiwara
authors.forename: Hideo
authors.initials: H
authors.lastname: Iwasaka
authors.forename: Kyosuke
authors.initials: K
authors.lastname: Kudo
authors.forename: Akira
authors.initials: A
authors.lastname: Hasegawa
authors.forename: Jyunya
authors.initials: J
authors.lastname: Kusaka
authors.forename: Tomohisa
authors.initials: T
authors.lastname: Uchida
authors.forename: Takayuki
authors.initials: T
authors.lastname: Noguchi
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000150:complications* / Q000188:drug therapy* / Q000378:metabolism; D004195:Disease Models, Animal; D006331:Heart Diseases / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D006334:Heart Function Tests / Q000187:drug effects; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007249:Inflammation / Q000139:chemically induced / Q000150:complications* / Q000378:metabolism; D007328:Insulin / Q000494:pharmacology*; D015850:Interleukin-6 / Q000097:blood; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D009566:Nitrates / Q000097:blood; D009573:Nitrites / Q000097:blood; D051381:Rats; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin; D015850:Interleukin-6; D008070:Lipopolysaccharides; D009566:Nitrates; D009573:Nitrites; D014409:Tumor Necrosis Factor-alpha