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Impact of Gender on the Myocardial Metabolic Response to Obesity

Linda R. Peterson, MD, FACC^_*,,,_*, Pablo F. Soto, MD^_*,, Pilar Herrero, ME, MS, B. Selma Mohammed, MD, PhD, Michael S. Avidan, MBBCh, Kenneth B. Schechtman, PhD^||, Carmen Dence, MS, Robert J. Gropler, MD, FACC^_*,

^_* Cardiovascular Division, Washington University School of Medicine, St. Louis, Missouri
Division of Geriatrics and Nutritional Sciences, Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri
Mallinckrodt Institute of Radiology, Washington University School of Medicine, St. Louis, Missouri
Department of Anesthesiology, Washington University School of Medicine, St. Louis, Missouri
^|| Division of Biostatistics, Washington University School of Medicine, St. Louis, Missouri.

^_* Address for correspondence: Dr. Linda R. Peterson, Washington University School of Medicine, Campus Box 8086, 660 S. Euclid Avenue, St. Louis, Missouri 63110. (Email: lpeterso{at}im.wustl.edu).

Objectives: We sought to determine the gender-specific effects of obesity on myocardial metabolism, work, and efficiency.

Background: Myocardial metabolism abnormalities may contribute to the development of obesity-related heart failure. Increased myocardial oxygen consumption (MVO₂) and fatty acid (FA) metabolism and decreased efficiency occur with obesity in women. It is unknown whether similar changes occur with obesity in men.

Methods: We quantified cardiac work, efficiency, myocardial blood flow (MBF), MVO₂, glucose, and FA metabolism with echocardiography and positron emission tomography in nonobese and obese men and women (N = 86).

Results: There were significant differences between the obese (n = 35) and nonobese (n = 51) subjects in age, body composition, plasma lipids, and insulin resistance in addition to differences between the men (n = 30) and women (n = 56) in body composition and plasma lipids. Female gender independently predicted increased cardiac work (p < 0.001). Female gender also related to lower efficiency (p < 0.05). Obesity and female gender independently predicted greater MBF (p < 0.01, p < 0.0005, respectively) and MVO₂ (p < 0.0005, p < 0.0001). Myocardial glucose uptake was not different among the 4 subject groups, but obesity and gender interacted in predicting glucose uptake (p < 0.05). Lower myocardial glucose utilization was independently predicted by female gender (p < 0.05), and it independently predicted lower myocardial glucose utilization/plasma insulin (p < 0.05). Obesity and gender significantly interacted in the determination of glucose utilization/plasma insulin (p = 0.01). There were no differences in FA uptake among the 4 groups, and although increasing obesity correlated with greater myocardial FA utilization and oxidation; female gender (p < 0.005, p < 0.01) and plasma triglycerides (p < 0.05, p < 0.005) were their independent predictors.

Conclusions: Women's and men's myocardial metabolic responses to obesity are not exactly the same. Obesity and gender modulate MBF and MVO₂, are related to myocardial substrate metabolism, and sometimes interact in its prediction. Gender modifies efficiency. Gender-related differences in myocardial metabolism may affect the development of/adaptation to obesity-related cardiac disease.

Key Words: positron emission tomography • gender • myocardial blood flow • myocardial metabolism • myocardial efficiency • obesity

Abbreviations and Acronyms   BMI = body mass index   FA = fatty acid   HOMA = homeostasis model assessment of insulin resistance   LV = left ventricular   MBF = myocardial blood flow   MVO2 = myocardial oxygen consumption   PET = positron emission tomography

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