Abstract
ContextAnorexia nervosa is a common illness among adolescents and is characterised by oxidative stress.ObjectiveThe effects of anorexia on mitochondrial function and redox state in leukocytes from anorexic subjects were evaluated.Design and settingA multi-centre, cross-sectional case-control study was performed.PatientsOur study population consisted of 20 anorexic patients and 20 age-matched controls, all of which were Caucasian women.Main outcome measuresAnthropometric and metabolic parameters were evaluated in the study population. To assess whether anorexia nervosa affects mitochondrial function and redox state in leukocytes of anorexic patients, we measured mitochondrial oxygen consumption, membrane potential, reactive oxygen species production, glutathione levels, mitochondrial mass, and complex I and III activity in polymorphonuclear cells.ResultsMitochondrial function was impaired in the leukocytes of the anorexic patients. This was evident in a decrease in mitochondrial O2 consumption (P<0.05), mitochondrial membrane potential (P<0.01) and GSH levels (P<0.05), and an increase in ROS production (P<0.05) with respect to control subjects. Furthermore, a reduction of mitochondrial mass was detected in leukocytes of the anorexic patients (P<0.05), while the activity of mitochondrial complex I (P<0.001), but not that of complex III, was found to be inhibited in the same population.ConclusionsOxidative stress is produced in the leukocytes of anorexic patients and is closely related to mitochondrial dysfunction. Our results lead us to propose that the oxidative stress that occurs in anorexia takes place at mitochondrial complex I. Future research concerning mitochondrial dysfunction and oxidative stress should aim to determine the physiological mechanism involved in this effect and the physiological impact of anorexia.
Highlights
Eating disorders are an increasingly frequent pathology that usually affects young women [1] and whose risk factors are varied and complex [2,3]
Mitochondrial function was impaired in the leukocytes of the anorexic patients
A reduction of mitochondrial mass was detected in leukocytes of the anorexic patients (P,0.05), while the activity of mitochondrial complex I (P,0.001), but not that of complex III, was found to be inhibited in the same population
Summary
Eating disorders are an increasingly frequent pathology that usually affects young women [1] and whose risk factors are varied and complex [2,3]. Anorexia nervosa (AN), the most severe of the three subtypes, is characterised by a significant and deliberate loss of weight, a distorted perception of one’s body and a pathological fear of being fat [4] It is often a chronic condition, especially in patients that have required hospital treatment [5], and is currently one of the most frequent disorders among adolescents [6]. Peripheral polymorphonuclear leukocytes (PMN) are inflammatory cells that, once activated, can release molecules that contribute to inflammation, endothelial impairment and oxidative stress They generate excessive amounts of ROS, which are harmful to cells, as they can initiate lipid peroxidation and apoptosis [9]. Their function and redox state in AN patients have not yet been determined
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