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Fat Oxidation before and after a High Fat Load in the Obese Insulin-Resistant State

Department of Human Biology, Nutrition and Toxicology Research Centre NUTRIM (E.E.B., G.H., W.H.M.S.), Maastricht University, Maastricht, The Netherlands; Department of Health and Nutrition (E.F.M.F.), National Institute of Public Health and the Environment, Bilthoven, The Netherlands; Institute of Preventive Medicine (C.V., C.H., T.I.S.), Danish Epidemiology Science Centre, Copenhagen University Hospital, Copenhagen, Denmark; Department of Sports Medicine (V.S., J.P.), Centre of Preventive Medicine, Third Faculty of Medicine, Charles University, Prague, Czech Republic; Department of Physiology and Nutrition (A.M.), University of Navarra, Pamplona, Spain; Institute of Human Nutrition (M.P., S.T., A.A.), The Royal Veterinary and Agricultural University, Copenhagen, Denmark; School of Biomedical Sciences (K.P., I.A.M.), Queens Medical Centre, University of Nottingham Medical School, Nottingham, United Kingdom; Department of Nutrition (J.M.O.), Hôtel-Dieu Hospital, Paris, France; Obesity Research Unit of the French Institute of Health and Medical Research U586 (P.B., D.L.), Louis Bugnard Institute and Clinical Investigation Centre, Toulouse University Hospitals, Paul Sabatier University, Toulouse, France; and Department of Medicine (I.A.), Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden

Address all correspondence and requests for reprints to: Dr. E. E. Blaak, Department of Human Biology, Nutrition Research Centre, Maastricht University, P.O. Box 616, 6200 MD Maastricht, The Netherlands. E-mail: e.blaak{at}hb.unimaas.nl.

Background: Obesity may be associated with a lowered use of fat as a fuel, which may contribute to the enlarged adipose tissue stores.

Aim: The aim of the present study was to study fatty acid use in the fasting state and in response to a high fat load in a large cohort of obese subjects (n = 701) and a lean reference group (n = 113).

Methods: Subjects from eight European centers underwent a test meal challenge containing 95 en% fat [energy content 50% of estimated resting energy expenditure (EE)]. Fasting and postprandial fat oxidation and circulating metabolites and hormones were determined over a 3-h period.

Results: Postprandial fat oxidation (as percent of postprandial EE, adjusted for fat mass, age, gender, center, and energy content of the meal) decreased with increasing body mass index (BMI) category (P < 0.01), an effect present only in those obese subjects with a relatively low fasting fat oxidation (below median, interaction BMI category x fasting fat oxidation, P < 0.001). Fasting fat oxidation increased with increasing BMI category (P < 0.001), which was normalized after adjustment for fat-free mass and fat mass. Furthermore, insulin resistance was positively associated with postprandial fat oxidation (P < 0.05) and negatively associated with fasting fat oxidation (expressed as percent of EE), independent of body composition.

Conclusions: The present data indicate an impaired capacity to regulate fat oxidation in the obese insulin-resistant state, which is hypothesized to play a role in the etiology of both obesity and insulin resistance.

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