Oxygen Consumption and Oxidative Capacity of Hepatocytes from Young Male Obese and Nonobese Zucker Rats

Abstract

The contribution of the liver to the increased metabolic efficiency of the obese rat Cfalfa) was examined. Oxygen consumption of isolated hepatocytes and isolated mitochondria, and hepatic activities of mitochondrial enzymes were measured. Hepatocyte oxygen consumption was similar in the obese and nonobese rats for all substrates tested. Mitochondria1 respiration also was similar in both phenotypes for all substrates tested. Activities of citrate synthase, succinate dehydrogenase, and cytochrome oxidase were similar for obese and nonobese rats. Taken together, these data show that in vitro hepatic oxygen consumption and oxidative capacity are similar in obese and nonobese rats. Rates of mitochondrial respiration with palmitoylcarnitine further show that the capacity for hepatic lipid oxidation is similar in obese and nonobese rats. Therefore, the increased metabolic efficiency of the obese rat probably cannot be attributed to an intrinsic decreased hepatic oxidative capacity. Further, there is no defect in hepatic lipid oxidative capacity in the young obese rat.

Melatonin reduces hepatic mitochondrial dysfunction in diabetic obese rats

“…We also noticed that melatonin increased the total mean area and number of the mitochondria in M-ZDF rats and their area in M-ZL, consistent with citrate synthase activity which was a common melatonin effect which restored hepatic mitochondria in ZDF rats to those in C-ZL group. This effect is consistent with findings obtained by Wardlaw and Kaplan [60] in obese Zucker rats and with our previous results in beige and white adipose tissue [19,70].…”

Fatty liver and insulin resistance in obese Zucker rats: No role for mitochondrial dysfunction

“…In the current study there was no difference in CS and COX activities between obese and lean Zucker rats in isolated mitochondria as well as in liver homogenate, indicating a similar relative amount of hepatic mitochondria and a similar oxidative capacity. The absence of variation of CS and COX activities is in agreement with the result obtained by Wardlaw and Kaplan [36] carried out on Zucker rats. The absence of mitochondrial dysfunction especially for the b-oxidation pathway was confirmed by the fact that serum b-hydroxybutyrate which is an indicator of liver b-oxidation capacity, was not altered in obese compared to lean Zucker rats.…”

Peroxisomal-mitochondrial oxidation in a rodent model of obesity-associated insulin resistance

“…Findings from the current investigation support this literature, as depressed hepatic citrate synthase activity and mitochondrial oxidation rates in the obese, insulinresistant condition were found and are indicative of diminished lipid disposal, which likely contributes to excessive lipid accumulation seen in this tissue. Previous investigations, however, have established that oxidation rates from isolated mitochondria are similar between lean and obese liver (5,10,70). Therefore, the diminished oxidation rates detected in the present study may not be due to inherent mitochondrial defects per se but rather may be partially explained by diminished mitochondrial content per tissue mass.…”