Decreased mitochondrial enzyme content in adipose tissue after the consumption of a high fat diet is associated with oxidative stress

Abstract

Based upon studies in genetically modified rodents it has been suggested that decreases in mitochondrial content and/or activity in abdominal adipose tissue is involved in the pathogenesis of obesity and type II diabetes. It is currently not known if diet induced obesity results in similar changes and if so the mechanisms involved. The purpose of the present study was to examine the effects of diet induced obesity on mitochondrial enzyme content in mouse abdominal adipose tissue and determine if these changes are associated with the induction of oxidative stress and reductions in PGC‐1 content and AMPK activity. Male C57Bl/6 were fed a high fat (~60% kcals fat) diet for 12 weeks. High fat feeding resulted in increases in body weight and percent body fat. The mitochondrial marker enzymes CS, COX I and COXIV were reduced ~30‐50% in epididymal fat pads from fat versus chow fed mice. The content of PGC‐1, a regulator of mitochondrial biogenesis, was reduced ~60% in fat pads from high fat fed mice. The phosphorylation of AMPK, a reputed mediator of mitochondrial biogenesis was reduced ~40% independent of changes in total enzyme content. The consumption of a high fat diet led to increases in protein carbonyls in visceral adipose tissue, suggesting the induction of oxidative stress. Collectively, these findings suggest an association between oxidative stress, reductions in AMPK‐PGC‐1 signaling and decreases in mitochondrial marker enzyme content in a model of diet induced obesity.