Elevated hepatic mitochondrial and peroxisomal oxidative capacities in fed and starved adult obese (ob/ob) mice

Abstract

Hepatic mitochondrial and peroxisomal oxidative capacities were studied in young (4-5 weeks old) and adult (6-9 months old) lean and obese ob/ob mice that were fed or starved for 24 or 48 h. The adult obese mice showed elevated capacity for mitochondrial oxidation (ng-atoms of O consumed/min per mg of protein) of lipid and non-lipid substrates, with the exception of pyruvate + malate, and elevated activities of citrate synthase and total carnitine palmitoyltransferase. Oxidative rates and enzyme activities were not affected by starvation of lean or obese mice, and both males and females responded similarly. Peroxisomal palmitoyl-CoA oxidation (nmol/min per mg of peroxisomal protein) was also increased in livers of adult obese mice and did not change with starvation. In young mice, hepatic mitochondrial and peroxisomal oxidative capacities in lean and obese mice were comparable. The increased mitochondrial and peroxisomal oxidative capacities appear to develop with maturation in obese ob/ob mice.

Activities of cytochrome c oxidase and citrate synthase in lymphocytes of obese and normal-weight subjects

“…1 Other studies showed that hepatic mitochondria from adult obese mice exhibit elevated capacity to oxidize nonlipid substrates. 2,52 This supports the notion that hepatic mitochondria from obese mice have an increased capacity to metabolize reducing equivalents, whether they are NAD þ -or FAD-linked. They also show elevated specific activity of CS and elevated capacity for mitochondrial and peroxisomal oxidation of lipid substrates.…”

A high-fat diet and regulatory T cells influence susceptibility to endotoxin-induced liver injury

“…In obesity and steatosis, increased fatty acid metabolism leads to increased mitochondrial respiratory activity and excessive production of mitochondrial reactive oxygen species (ROS) in the liver, 8,28 which are known to regulate T-cell apoptosis. 29 High levels of ROS probably kill cells directly, whereas low levels probably mediate apoptosis indirectly through their effects on signal transduction and gene expression.…”

Mechanism for obesity-induced increase in myocardial lipid peroxidation

“…17 Theoretically, it is possible that all of these mechanisms are present and participate in the increase in myocardial lipid peroxidation in obesity. Nonetheless, to date, there is no experimental evidence regarding which of these mechanisms are contributors to the myocardial oxidative damage associated with obesity.…”