Impaired skeletal muscle mitochondrial function in morbidly obese patients is normalized one year after bariatric surgery

Background: Obesity and type 2 diabetes are associated with impaired skeletal muscle mitochondrial metabolism. As an intrinsic characteristic of an individual, skeletal muscle mitochondrial dysfunction could be a risk factor for weight gain and obesity-associated co-morbidities, such as type 2 diabetes. On the other hand, impaired skeletal muscle metabolism could be a consequence of obesity. We hypothesize that marked weight loss after bariatric surgery recovers skeletal muscle mitochondrial function. Methods: Skeletal muscle mitochondrial function as assessed by high-resolution respirometry was measured in 8 morbidly obese patients (body mass index [BMI], 41.3 +/- 4.7 kg/m(2); body fat, 48.3% +/- 5.2%) before and 1 year after bariatric surgery (mean weight loss: 35.0 +/- 8.6 kg). The results were compared with a lean (BMI 22.8 +/- 1.1 kg/m(2); body fat, 15.6% +/- 4.7%) and obese (BMI 33.5 +/- 4.2 kg/m(2); body fat, 34.1% +/- 6.3%) control group. Results: Before surgery, adenosine diphosphate (ADP)-stimulated (state 3) respiration on glutamate/succinate was decreased compared with lean patients (9.5 +/- 2.4 versus 15.6 +/- 4.4 O-2 flux/mtDNA; P < .05). One year after surgery, mitochondrial function was comparable to that of lean controls (after weight loss, 12.3 +/- 5.5; lean, 15.6 +/- 4.4 O-2 flux/mtDNA). In addition, we observedan increased state 3 respiration on a lipid substrate after weight loss (10.0 +/- 3.2 versus 14.0 +/- 6.6 O-2 flux/mtDNA; P < .05). Conclusion: We conclude that impaired skeletal muscle mitochondrial function is a consequence of obesity that recovers after marked weight loss. (Surg Obes Relat Dis 2013;9:936-941.) (c) 2013 American Society for Metabolic and Bariatric Surgery. All rights reserved.