Energy restriction in obese subjects impact differently two mitochondrial function markers |
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Authors: | A B Crujeiras D Parra E Goyenechea I Abete P González-Muniesa J A Martínez |
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Institution: | (1) Department of Nutrition and Food Sciences, Physiology and Toxicology, University of Navarra, C/ Irunlarrea 1, 31008 Pamplona, Spain |
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Abstract: | Excessive fat deposition is the key feature in obesity, which is empowered by cytokines overproduction and stimulation of
cell oxidative stress processes, but little is known about energy availability in the form of ATP and mitochondrial function
in the obese subjects. Thus, the aim of this study was to evaluate the possible changes in energy metabolism after a 8-weeks
balanced-hypocaloric diet in obese subjects by measuring the ATP-content in leukocytes, by assessing 2-keto 1-13C] isocaproate breath test (KICA-BT) parameters related to mitochondrial function and by analyzing inflammatory and oxidative
stress biomarkers. All the recruited obese subjects (n=19) lost body weight after dieting (−5.55±2.88%). The hypocaloric treatment
induced a decrease in leptin levels and lipid peroxidation markers. Interestingly, the ATP content in blood leukocytes increased
(49.9±32.5 vs 36.2±27.9 pmol/mg prot.; p<0.05), while KICA tracer mitochondrial oxidation decreased (30.9±5.9 vs. 33.1±4.5%13C; p<0.05) after weight loss. These results show that two minimally invasive methods were able to detect changes in mitochondrial
function as induced by a hypocaloric diet, which is of great interest in order to understand oxidative processes associated
with weight homeostasis as well as to establish newer anti-obesity therapeutic targets by using mitochondrial function markers
in vivo. |
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Keywords: | |
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