Energy restriction in obese subjects impact differently two mitochondrial function markers

ABSTRACT

Excessive fat deposition is the key feature in obesity, which is empowered bycytokines overproduction and stimulation of cell oxidative stress processes, but littleis known about energy availability in the form of ATP and mitochondrial functionin the obese subjects. Thus, the aim of this study was to evaluate the possible changesin energy metabolism after a 8-weeks balanced-hypocaloric diet in obese subjects bymeasuring the ATP-content in leukocytes, by assessing 2-keto[1-13C]isocaproatebreath test (KICA-BT) parameters related to mitochondrial function and by analyzinginflammatory and oxidative stress biomarkers. All the recruited obese subjects(n=19) lost body weight after dieting (-5.55±2.88%). The hypocaloric treatmentinduced a decrease in leptin levels and lipid peroxidation markers. Interestingly, theATP 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 invasivemethods were able to detect changes in mitochondrial function as induced by ahypocaloric diet, which is of great interest in order to understand oxidative processesassociated with weight homeostasis as well as to establish newer anti-obesity therapeutictargets by using mitochondrial function markers in vivo (AU)

RESUMEN

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