title: Effect of obesity and insulin resistance on myocardial substrate metabolism and efficiency in young women.
abstract: BACKGROUND
  Obesity is a risk factor for impaired cardiac performance, particularly in women. Animal studies suggest that alterations in myocardial fatty acid metabolism and efficiency in obesity can cause decreased cardiac performance. In the present study, we tested the hypothesis that myocardial fatty acid metabolism and efficiency are abnormal in obese women.
  
  
  RESULTS
  We studied 31 young women (body mass index [BMI] 19 to 52 kg/m2); 19 were obese (BMI >30 kg/m2). Myocardial oxygen consumption (MVO2) and fatty acid uptake (MFAUp), utilization (MFAU), and oxidation (MFAO) were quantified by positron emission tomography. Cardiac work was measured by echocardiography, and efficiency was calculated as work/MVO2. BMI correlated with MVO2 (r=0.58, P=0.0006), MFAUp (r=0.42, P<0.05), and efficiency (r=-0.40, P<0.05). Insulin resistance, quantified by the glucose area under the curve (AUC) during an oral glucose tolerance test, correlated with MFAUp (r=0.55, P<0.005), MFAU (r=0.62, P<0.001), and MFAO (r=0.58, P<0.005). A multivariate, stepwise regression analysis showed that BMI was the only independent predictor of MVO2 and efficiency (P=0.0005 and P<0.05, respectively). Glucose AUC was the only independent predictor of MFAUp, MFAU, and MFAO (P<0.05, <0.005, and <0.005, respectively).
  
  
  CONCLUSIONS
  In young women, obesity is a significant predictor of increased MVO2 and decreased efficiency, and insulin resistance is a robust predictor of MFAUp, MFAU, and MFAO. This increase in fatty acid metabolism and decrease in efficiency is concordant with observations made in experimental models of obesity. These metabolic changes may play a role in the pathogenesis of decreased cardiac performance in obese women.
authors.affiliation: Department of Medicine, Division of Cardiology, Washington University School of Medicine, Campus Box 8086, 660 S Euclid Ave, St Louis, MO 63110, USA. lpeterso@im.wustl.edu
authors.forename: Linda R
authors.initials: LR
authors.lastname: Peterson
authors.forename: Pilar
authors.initials: P
authors.lastname: Herrero
authors.forename: Kenneth B
authors.initials: KB
authors.lastname: Schechtman
authors.forename: Susan B
authors.initials: SB
authors.lastname: Racette
authors.forename: Alan D
authors.initials: AD
authors.lastname: Waggoner
authors.forename: Zulia
authors.initials: Z
authors.lastname: Kisrieva-Ware
authors.forename: Carmen
authors.initials: C
authors.lastname: Dence
authors.forename: Samuel
authors.initials: S
authors.lastname: Klein
authors.forename: JoAnn
authors.initials: J
authors.lastname: Marsala
authors.forename: Timothy
authors.initials: T
authors.lastname: Meyer
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Gropler
mesh_terms: D000328:Adult; D019540:Area Under Curve; D001786:Blood Glucose / Q000032:analysis; D015992:Body Mass Index; D002302:Cardiac Output; D004452:Echocardiography; D004734:Energy Metabolism; D005227:Fatty Acids / Q000378:metabolism*; D005260:Female; D005947:Glucose / Q000378:metabolism; D005951:Glucose Tolerance Test; D006321:Heart / Q000000981:diagnostic imaging; D006439:Hemodynamics; D006801:Humans; D007333:Insulin Resistance; D009206:Myocardium / Q000378:metabolism*; D009765:Obesity / Q000150:complications / Q000378:metabolism*; D010101:Oxygen Consumption; D017697:Premenopause; D014055:Tomography, Emission-Computed; D018487:Ventricular Dysfunction, Left / Q000209:etiology*
chemical_list: D001786:Blood Glucose; D005227:Fatty Acids; D005947:Glucose