Markers of capacity to utilize fatty acids in human skeletal muscle: relation to insulin resistance and obesity and effects of weight loss

“…Insulin-stimulated glucose disposal measured during a 3-h euglycemic-hyperinsulinemic clamp was markedly lower in obese type 2 diabetic and nondiabetic subjects when compared with the lean controls (Table 1), indicating a state of insulin resistance. In keeping with previous reports (9,41), glucose oxidation during the insulin clamp was significantly reduced in obese subjects and in type 2 diabetic patients (data not shown).…”

“…In line with these results, the activity of citrate synthase, beta-hydroxyacyl-CoA dehydrogenase and cytochrome C oxidase II activity did not change in response to interventions. Our results are in agreement with previous reports indicating oxidative enzyme activity does not improve after weight loss in obese humans [50,51]. Taken together, our results suggest: (1) caloric restriction induces the proliferation of mitochondria with “efficient” electron transport systems coupled to lower whole-body oxygen consumption, and (2) mtDNA or other nonenzymatic markers of mitochondrial mass (i.e., mitochondrial structural proteins such as cardiolipin [52]) may be better indicators of mitochondrial content than enzyme activities under caloric restriction conditions in humans.…”

“…This is in agreement with previously reported findings [18,36] after moderate weight loss, demonstrating that even massive weight reduction is without effect on CPT1 expression. In contrast to physical exercise-mediated PGC1A upregulation, PGC1A upregulation due to weight reduction was not associated with an increase of CPT1 expression.…”