- 作者：Guy H.E.J. Vijgen ; Nicole D. Bouvy ; Joris Hoeks ; S ; er Wijers ; Patrick Schrauwen ; Wouter D. van Marken Lichtenbelt
- 关键词：Morbid obesity ; Weight loss ; Skeletal muscle mitochondrial function ; Gastric banding
- 刊名：Surgery for Obesity and Related Diseases
- 出版年：November-December, 2013
- 年：2013
- 卷：9
- 期：6
- 页码：936-941
- 全文大小：534 K
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卤4.7 kg/m2; body fat, 48.3%卤5.2%) before and 1 year after bariatric surgery (mean weight loss: 35.0卤8.6 kg). The results were compared with a lean (BMI 22.8卤1.1 kg/m2; body fat, 15.6%卤4.7%) and obese (BMI 33.5卤4.2 kg/m2; body fat, 34.1%卤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卤2.4 versus 15.6卤4.4 O2 flux/mtDNA; P<.05). One year after surgery, mitochondrial function was comparable to that of lean controls (after weight loss, 12.3卤5.5; lean, 15.6卤4.4 O2 flux/mtDNA). In addition, we observed an increased state 3 respiration on a lipid substrate after weight loss (10.0卤3.2 versus 14.0卤6.6 O2 flux/mtDNA; P< .05).
Conclusion
We conclude that impaired skeletal muscle mitochondrial function is a consequence of obesity that recovers after marked weight loss.