Patients with type 2 diabetes have normal mitochondrial function in skeletal muscle.
Patients with type 2 diabetes have normal mitochondrial function in skeletal muscle.
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DOI：
10.1007/s00125-007-0594-3
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发表时间：
2007-04
期刊：
影响因子：
8.2
通讯作者：
Dela, F.
中科院分区：
文献类型：
--
作者：
Boushel, R.;Gnaiger, E.;Schjerling, P.;Skovbro, M.;Kraunsoe, R.;Dela, F.
胰岛素抵抗和2型糖尿病与线粒体功能障碍有关。本研究的目的是验证这一假说，即2型糖尿病受试者骨骼肌中的氧化磷酸化和电子传递能力由于线粒体含量的减少而降低。采用高分辨率呼吸法测定健康人(n = 8；年龄58 ± 2岁；BMI 28 ± 1；空腹血糖5.4 ± 0.2 mm ol/L)和2型糖尿病患者(n = 11；年龄62 ± 2岁；BMI 32 ± 2 m ol/m2；空腹血糖9.0 ± 0.8 m ol/L)股四头肌组织通透性纤维的氧通量。在腺苷二磷酸刺激的状态3呼吸中，2型糖尿病患者每毫克肌肉(鲜重)的氧流量较低(p <； 0.0 5)，在有复合体I底物(谷氨酸)存在的情况下(31 ± 2vs 43 ± 3 pmolO2 S−1 mg−1)，以及在谷氨酸+琥珀酸(来自络合物I和II的平行电子输入)的反应下(63 ± 3vs 85 ± 6 pmolS−1 mg−1)。经FCCP去偶联后，2型糖尿病患者的氧通量进一步增加，但仍低于健康对照组(86 ± 4 vs 10 9 ± 8 pmol S−1 mg−1)。然而，当线粒体DNA含量或柠檬酸合成酶活性的氧流量正常化后，2型糖尿病患者和健康对照组之间的氧化磷酸化或电子传递能力没有差异。2型糖尿病患者线粒体功能正常。2型糖尿病患者的偶联和非偶联呼吸迟钝可归因于线粒体含量较低。
Insulin resistance and type 2 diabetes are associated with mitochondrial dysfunction. The aim of the present study was to test the hypothesis that oxidative phosphorylation and electron transport capacity are diminished in the skeletal muscle of type 2 diabetic subjects, as a result of a reduction in the mitochondrial content. The O2 flux capacity of permeabilised muscle fibres from biopsies of the quadriceps in healthy subjects (n = 8; age 58 ± 2 years [mean±SEM]; BMI 28 ± 1 kg/m2; fasting plasma glucose 5.4 ± 0.2 mmol/l) and patients with type 2 diabetes (n = 11; age 62 ± 2 years; BMI 32 ± 2 kg/m2; fasting plasma glucose 9.0 ± 0.8 mmol/l) was measured by high-resolution respirometry. O2 flux expressed per mg of muscle (fresh weight) during ADP-stimulated state 3 respiration was lower (p < 0.05) in patients with type 2 diabetes in the presence of complex I substrate (glutamate) (31 ± 2 vs 43 ± 3 pmol O2 s−1 mg−1) and in response to glutamate + succinate (parallel electron input from complexes I and II) (63 ± 3 vs 85 ± 6 pmol s−1 mg−1). Further increases in O2 flux capacity were observed in response to uncoupling by FCCP, but were again lower (p < 0.05) in type 2 diabetic patients than in healthy control subjects (86 ± 4 vs 109 ± 8 pmol s−1 mg−1). However, when O2 flux was normalised for mitochondrial DNA content or citrate synthase activity, there were no differences in oxidative phosphorylation or electron transport capacity between patients with type 2 diabetes and healthy control subjects. Mitochondrial function is normal in type 2 diabetes. Blunting of coupled and uncoupled respiration in type 2 diabetic patients can be attributed to lower mitochondrial content.
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影响因子：
158.5
作者：
Knowler, WC;Barrett-Connor, E;Nathan, DM
通讯作者：
Nathan, DM
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：
Short, KR;Vittone, JL;Nair, KS
通讯作者：
Nair, KS
影响因子：
15.9
作者：
Morino, K;Petersen, KF;Shulman, GI
通讯作者：
Shulman, GI
影响因子：
8.2
作者：
ERIKSSON, KF;LINDGARDE, F
通讯作者：
LINDGARDE, F