title: Insulin resistance is not associated with myocardial steatosis in women.
abstract: OBJECTIVE
  Insulin resistance, an independent risk-factor for cardiovascular disease, precedes type 2 diabetes and is associated with ectopic lipid accumulation in skeletal muscle and liver. Recent evidence indicates that cardiac steatosis plays a central role in the development of diabetic cardiomyopathy. However, it is not known whether insulin resistance as such in the absence of type 2 diabetes is associated with heart steatosis and/or impaired function. We therefore assessed myocardial steatosis and myocardial function in a sample of women with normal insulin sensitivity, insulin resistance, impaired glucose tolerance (IGT) and type 2 diabetes.
  
  
  METHODS
  Magnetic resonance imaging and localised spectroscopy were used to measure left ventricular dynamic variables and myocardial lipid accumulation in interventricular septum of non-diabetic, age- and BMI-matched insulin-sensitive (n = 11, 47 ± 6 years, BMI 25 ± 2 kg/m(2); clamp-like index [CLIX] = 9.7 ± 0.7) and insulin-resistant (n = 10, 48 ± 5 years, 27 ± 4 kg/m(2); CLIX = 4.5 ± 0.4) women with normal glucose tolerance as well as of women with IGT (n = 6, 45 ± 5 years, 28 ± 6 kg/m(2); CLIX = 3.6 ± 1.1) and type 2 diabetes (n = 7, 52 ± 10 years, 27 ± 3 kg/m(2)).
  
  
  RESULTS
  Myocardial lipid content was increased in type 2 diabetic women only (insulin-sensitive 0.4 ± 0.2% [means ± SD]; insulin-resistant 0.4 ± 0.1%; IGT 0.5 ± 0.2%; type 2 diabetes 0.7 ± 0.3%; p < 0.05). In insulin-resistant and type 2 diabetic women, stroke volume was lower (-15% and -27%, respectively, vs insulin-sensitive) and heart rate was higher (11% and 14%, respectively, vs insulin-sensitive, p < 0.05). No other differences in systolic and diastolic function were observed between study groups.
  
  
  CONCLUSIONS
  In contrast to liver and skeletal muscle, insulin resistance as such is not associated with increased myocardial lipid accumulation.
authors.affiliation: Division of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Währinger Gürtel 18-20, 1090 Wien, Austria.
authors.forename: M
authors.initials: M
authors.lastname: Krššák
authors.forename: Y
authors.initials: Y
authors.lastname: Winhofer
authors.forename: C
authors.initials: C
authors.lastname: Göbl
authors.forename: M
authors.initials: M
authors.lastname: Bischof
authors.forename: G
authors.initials: G
authors.lastname: Reiter
authors.forename: A
authors.initials: A
authors.lastname: Kautzky-Willer
authors.forename: A
authors.initials: A
authors.lastname: Luger
authors.forename: M
authors.initials: M
authors.lastname: Krebs
authors.forename: C
authors.initials: C
authors.lastname: Anderwald
mesh_terms: D000328:Adult; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism / Q000473:pathology; D005260:Female; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D009682:Magnetic Resonance Spectroscopy; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology*