Altered mitochondrial function and oxidative stress in leukocytes of anorexia nervosa patients.

PLoS One

Foundation for the Promotion of Healthcare and Biomedical Research in the Valencian Community (FISABIO), Valencia, Spain; Service of Endocrinology, University Hospital Doctor Peset, Valencia, Spain; Institute of Health Research INCLIVA, University of Valencia, Valencia, Spain; Department of Medicine, University of Valencia, Valencia, Spain.

Published: June 2015

Context: Anorexia nervosa is a common illness among adolescents and is characterised by oxidative stress.

Objective: The effects of anorexia on mitochondrial function and redox state in leukocytes from anorexic subjects were evaluated.

Design And Setting: A multi-centre, cross-sectional case-control study was performed.

Patients: Our study population consisted of 20 anorexic patients and 20 age-matched controls, all of which were Caucasian women.

Main Outcome Measures: Anthropometric 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.

Results: Mitochondrial 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.

Conclusions: Oxidative 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.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4177818PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0106463PLOS

Publication Analysis

Top Keywords

mitochondrial function
16
anorexia nervosa
12
leukocytes anorexic
12
anorexic patients
12
function redox
8
redox state
8
state leukocytes
8
study population
8
mitochondrial
6
altered mitochondrial
4

Similar Publications

Background: The endangered Kashmir musk deer (Moschus cupreus), native to high-altitude Himalayas, is an ecological significant and endangered ungulate, threatened by habitat loss and poaching for musk pod distributed in western Himalayan ranges of India, Nepal and Afghanistan. Despite its critical conservation status and ecological importance in regulating vegetation dynamics, knowledge gaps persist regarding its population structure and genetic diversity, hindering effective management strategies.

Methods And Results: We aimed to understand the population genetics of Kashmir musk deer in north-western Himalayas using two mitochondrial DNA (mtDNA) regions and 11 microsatellite loci.

View Article and Find Full Text PDF

The complex interaction between circadian rhythms and physiological functions is essential for maintaining human health. At the heart of this interaction lies the PERIOD proteins (PERs), pivotal to the circadian clock, influencing the timing of physiological and behavioral processes and impacting oxidative stress, immune functionality, and tumorigenesis. PER1 orchestrates the cooperation of the enzyme GPX1, modulating mitochondrial dynamics in sync with daily rhythms and oxidative stress, thus regulating the mechanisms managing energy substrates.

View Article and Find Full Text PDF

Parthenolide improves sepsis-induced coagulopathy by inhibiting mitochondrial-mediated apoptosis in vascular endothelial cells through BRD4/BCL-xL pathway.

J Transl Med

January 2025

Department of Anesthesiology, Daping Hospital, Army Medical University, No.10, Changjiang Road, Yuzhong District, Chongqing, 400042, China.

Background: Sepsis is a systemic inflammatory syndrome that can cause coagulation abnormalities, leading to damage in multiple organs. Vascular endothelial cells (VECs) are crucial in the development of sepsis-induced coagulopathy (SIC). The role of Parthenolide (PTL) in regulating SIC by protecting VECs remains unclear.

View Article and Find Full Text PDF

Background: Glioblastoma (GBM) is a lethal brain tumor characterized by the glioma stem cell (GSC) niche. The V-ATPase proton pump has been described as a crucial factor in sustaining GSC viability and tumorigenicity. Here we studied how patients-derived GSCs rely on V-ATPase activity to sustain mitochondrial bioenergetics and cell growth.

View Article and Find Full Text PDF

Objective: Long-term management of people living with HIV (PLWHs) often relies on CD4 T cell counts for assessing immune recovery, yet a single metric offers limited information. This study aimed to explore the association between the CD4/CD8 ratio and T lymphocyte activities in PLWHs.

Methods: 125 PLWHs and 31 HIV-uninfected controls (UCs) were enrolled and categorized into four groups based on their CD4/CD8 ratios: extremely low ratio (ELR) group: 0.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!