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Ellen E. Blaak, Gabby Hul, Camilla Verdich, Vladimir Stich, Alfredo Martinez, Martin Petersen, Edith F. M. Feskens, Kishor Patel, Jean Michel Oppert, Pierre Barbe, Søren Toubro, Ingalena Anderson, Jan Polak, Arne Astrup, Ian A. Macdonald, Dominique Langin, Claus Holst, Thorkild I. Sørensen, Wim H. M. Saris, Fat Oxidation before and after a High Fat Load in the Obese Insulin-Resistant State, The Journal of Clinical Endocrinology & Metabolism, Volume 91, Issue 4, 1 April 2006, Pages 1462–1469, https://doi.org/10.1210/jc.2005-1598
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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 × 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.