Restoration of muscle mitochondrial function and metabolic flexibility in type 2 diabetes by exercise training is paralleled by increased myocellular fat storage and improved insulin sensitivity.
Restoration of muscle mitochondrial function and metabolic flexibility in type 2 diabetes by exercise training is paralleled by increased myocellular fat storage and improved insulin sensitivity.
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DOI：
10.2337/db09-1322
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发表时间：
2010-03
期刊：
影响因子：
7.7
通讯作者：
Hesselink MK
中科院分区：
文献类型：
--
作者：
Meex RC;Schrauwen-Hinderling VB;Moonen-Kornips E;Schaart G;Mensink M;Phielix E;van de Weijer T;Sels JP;Schrauwen P;Hesselink MK
线粒体功能障碍和骨骼肌脂肪积累（增加细胞内脂质[IMCL]）与2型糖尿病的发展有关。我们研究了运动训练是否可以恢复2型糖尿病患者的线粒体功能和胰岛素敏感性。18名男性2型糖尿病患者和20名体重、BMI、年龄和最大摄氧量相当的健康男性对照受试者参加了为期12周的联合渐进式训练计划（每周三次，每次45分钟）。在训练前后测量体内线粒体功能（通过磁共振波谱评估）、胰岛素敏感性（钳形法）、代谢柔韧性（间接量热法）和IMCL含量（组织化学）。2型糖尿病患者线粒体功能较对照组降低（P = 0.03），对照组经训练后线粒体功能改善（提高28%，P = 0.02）， 2型糖尿病患者线粒体功能恢复到对照组水平（提高48%，P < 0.01）。对照组胰岛素敏感性有改善趋势（δ Rd升高8%，P = 0.08）， 2型糖尿病患者胰岛素敏感性有明显改善（δ Rd升高63%，P < 0.01）。两组胰岛素刺激的内源性葡萄糖生成抑制均得到改善（对照组为- 64%，P < 0.01；糖尿病组为- 52%，P < 0.01）。训练后，2型糖尿病患者的代谢灵活性得到恢复（δ呼吸交换比增加63%，P = 0.01），而对照组的代谢灵活性没有变化（δ呼吸交换比增加7%，P = 0.22）。从训练前的IMCL水平开始，训练倾向于增加2型糖尿病患者的IMCL含量（增加27%，P = 0.10），特别是在2型肌肉纤维中。运动训练可恢复2型糖尿病患者体内线粒体功能。胰岛素介导的葡萄糖处理和代谢灵活性在2型糖尿病患者面对近显著增加的IMCL含量时得到改善。这表明IMCL储存能力的增加和线粒体功能改善的恢复有助于改善肌肉胰岛素敏感性。
Mitochondrial dysfunction and fat accumulation in skeletal muscle (increased intramyocellular lipid [IMCL]) have been linked to development of type 2 diabetes. We examined whether exercise training could restore mitochondrial function and insulin sensitivity in patients with type 2 diabetes. Eighteen male type 2 diabetic and 20 healthy male control subjects of comparable body weight, BMI, age, and Vo2max participated in a 12-week combined progressive training program (three times per week and 45 min per session). In vivo mitochondrial function (assessed via magnetic resonance spectroscopy), insulin sensitivity (clamp), metabolic flexibility (indirect calorimetry), and IMCL content (histochemically) were measured before and after training. Mitochondrial function was lower in type 2 diabetic compared with control subjects (P = 0.03), improved by training in control subjects (28% increase; P = 0.02), and restored to control values in type 2 diabetic subjects (48% increase; P < 0.01). Insulin sensitivity tended to improve in control subjects (delta Rd 8% increase; P = 0.08) and improved significantly in type 2 diabetic subjects (delta Rd 63% increase; P < 0.01). Suppression of insulin-stimulated endogenous glucose production improved in both groups (−64%; P < 0.01 in control subjects and −52% in diabetic subjects; P < 0.01). After training, metabolic flexibility in type 2 diabetic subjects was restored (delta respiratory exchange ratio 63% increase; P = 0.01) but was unchanged in control subjects (delta respiratory exchange ratio 7% increase; P = 0.22). Starting with comparable pretraining IMCL levels, training tended to increase IMCL content in type 2 diabetic subjects (27% increase; P = 0.10), especially in type 2 muscle fibers. Exercise training restored in vivo mitochondrial function in type 2 diabetic subjects. Insulin-mediated glucose disposal and metabolic flexibility improved in type 2 diabetic subjects in the face of near–significantly increased IMCL content. This indicates that increased capacity to store IMCL and restoration of improved mitochondrial function contribute to improved muscle insulin sensitivity.
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影响因子：
8.2
作者：
Krssak, M;Petersen, KF;Roden, M
通讯作者：
Roden, M
胰岛素2型糖尿病父母的胰岛素耐药后代的胰岛素刺激的ATP合成和磷酸盐转运减少。
影响因子：
15.8
作者：
Petersen, KF;Dufour, S;Shulman, GI
通讯作者：
Shulman, GI
影响因子：
5.8
作者：
Goodpaster, BH;He, J;Kelley, DE
通讯作者：
Kelley, DE
DOI：
10.1073/pnas.1032913100
发表时间：
2003-07-08
影响因子：
11.1
作者：
Patti, ME;Butte, AJ;Mandarino, LJ
通讯作者：
Mandarino, LJ
影响因子：
7.7
作者：
Kelley, DE;Mandarino, LJ
通讯作者：
Mandarino, LJ