title: Contribution of glucose tolerance and gender to cardiac adiposity.
abstract: OBJECTIVE
  To examine whether pericardial and myocardial fat depots may contribute to the association between diabetes and cardiovascular risk, including sex-related differences, and the role of adiponectin, we evaluated data in patients with obesity and without diabetes [nondiabetic (ND)] or with impaired glucose tolerance or type 2 diabetes and in lean ND controls.
  
  
  METHODS
  Magnetic resonance imaging and spectroscopy were used to measure left ventricular (LV) function and abdominal sc and visceral fat areas to estimate respective masses, pericardial fat depots, and myocardial triglyceride content in 53 subjects (10 lean ND, 25 obese ND, six impaired-glucose-tolerance, and 12 type 2 diabetic patients with macrovascular disease); gender effects and adiponectin levels were evaluated in the available subset of subjects.
  
  
  RESULTS
  Myocardial and pericardial fat increased progressively across study groups. They were lower in obese women than men (P = 0.002), but cardiac steatosis caught up in hyperglycemic women (+81% vs. ND, P = 0.01). Adiponectin was inversely related with both fat depots (P < 0.01) and LV mass (P = 0.003) and positively with LV function (P = 0.03). In multiple regression analysis, myocardial and pericardial fat were independently related with plasma glucose levels, only pericardial fat mass was associated with visceral adiposity and myocardial fat with cardiac output and work.
  
  
  CONCLUSIONS
  We conclude that glycemia, gender, adiponectin, and cardiac workload are associated with, and hyperglycemia and male gender are independent positive predictors of, heart adiposity. Once glucose tolerance becomes impaired, the evolution of cardiac steatosis is more pronounced in women.
authors.affiliation: Turku PET Centre, University of Turku, 20521 Turku, Finland. patricia.iozzo@ifc.cnr.it
authors.forename: Patricia
authors.initials: P
authors.lastname: Iozzo
authors.forename: Riikka
authors.initials: R
authors.lastname: Lautamaki
authors.forename: Ronald
authors.initials: R
authors.lastname: Borra
authors.forename: Hanna-Riikka
authors.initials: HR
authors.lastname: Lehto
authors.forename: Marco
authors.initials: M
authors.lastname: Bucci
authors.forename: Antti
authors.initials: A
authors.lastname: Viljanen
authors.forename: Jussi
authors.initials: J
authors.lastname: Parkka
authors.forename: Virva
authors.initials: V
authors.lastname: Lepomaki
authors.forename: Romina
authors.initials: R
authors.lastname: Maggio
authors.forename: Riitta
authors.initials: R
authors.lastname: Parkkola
authors.forename: Juhani
authors.initials: J
authors.lastname: Knuuti
authors.forename: Pirjo
authors.initials: P
authors.lastname: Nuutila
mesh_terms: D000273:Adipose Tissue / Q000033:anatomy & histology*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000473:pathology; D005260:Female; D018149:Glucose Intolerance / Q000097:blood* / Q000473:pathology; D005951:Glucose Tolerance Test; D006321:Heart / Q000033:anatomy & histology*; D006801:Humans; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D009206:Myocardium / Q000378:metabolism; D009765:Obesity / Q000097:blood* / Q000473:pathology; D014280:Triglycerides / Q000378:metabolism; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology; D016277:Ventricular Function, Left / Q000502:physiology
chemical_list: D014280:Triglycerides