• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The New England journal of medicine >Impaired mitochondrial activity in the insulin-resistant offspring of patients with type 2 diabetes.
【24h】

Impaired mitochondrial activity in the insulin-resistant offspring of patients with type 2 diabetes.

机译：2型糖尿病患者胰岛素抵抗后代的线粒体活性受损。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

BACKGROUND: Insulin resistance appears to be the best predictor of the development of diabetes in the children of patients with type 2 diabetes, but the mechanism responsible is unknown. METHODS: We performed hyperinsulinemic-euglycemic clamp studies in combination with infusions of [6,6-(2)H(2)]glucose in healthy, young, lean, insulin-resistant offspring of patients with type 2 diabetes and insulin-sensitive control subjects matched for age, height, weight, and physical activity to assess the sensitivity of liver and muscle to insulin. Proton ((1)H) magnetic resonance spectroscopy studies were performed to measure intramyocellular lipid and intrahepatic triglyceride content. Rates of whole-body and subcutaneous fat lipolysis were assessed by measuring the rates of [(2)H(5)]glycerol turnover in combination with microdialysis measurements of glycerol release from subcutaneous fat. We performed (31)P magnetic resonance spectroscopy studies to assess the rates of mitochondrial oxidative-phosphorylation activity in muscle. RESULTS: The insulin-stimulated rate of glucose uptake by muscle was approximately 60 percent lower in the insulin-resistant subjects than in the insulin-sensitive control subjects (P<0.001) and was associated with an increase of approximately 80 percent in the intramyocellular lipid content (P=0.005). This increase in intramyocellular lipid content was most likely attributable to mitochondrial dysfunction, as reflected by a reduction of approximately 30 percent in mitochondrial phosphorylation (P=0.01 for the comparison with controls), since there were no significant differences in systemic or localized rates of lipolysis or plasma concentrations of tumor necrosis factor alpha, interleukin-6, resistin, or adiponectin. CONCLUSIONS: These data support the hypothesis that insulin resistance in the skeletal muscle of insulin-resistant offspring of patients with type 2 diabetes is associated with dysregulation of intramyocellular fatty acid metabolism, possibly because of an inherited defect in mitochondrial oxidative phosphorylation.
机译：背景：胰岛素抵抗似乎是2型糖尿病患者儿童糖尿病发展的最佳预测指标，但其作用机理尚不清楚。方法：我们进行了高胰岛素-正常血糖钳夹研究，并联合输注了[6,6-（2）H（2）]葡萄糖在2型糖尿病患者中的健康，年轻，瘦弱，胰岛素抵抗的后代并进行了胰岛素敏感性控制根据年龄，身高，体重和体育活动对受试者进行匹配，以评估肝脏和肌肉对胰岛素的敏感性。进行质子（（1）H）磁共振波谱研究以测量肌内脂质和肝内甘油三酸酯含量。通过测量[（2）H（5）]甘油更新率并结合微量透析测量从皮下脂肪中释放出的甘油来评估全身和皮下脂肪脂解的速率。我们进行了（31）P磁共振波谱研究，以评估肌肉中线粒体氧化磷酸化活性的速率。结果：在胰岛素抵抗患者中，胰岛素刺激的肌肉葡萄糖摄取速率比对胰岛素敏感的对照组低约60％（P <0.001），并且与肌内脂质增加约80％有关含量（P = 0.005）。肌细胞内脂质含量的这种增加很可能归因于线粒体功能障碍，反映为线粒体磷酸化水平降低了约30％（与对照组相比，P = 0.01），因为全身或局部脂解速率没有显着差异或血浆中肿瘤坏死因子α，白介素6，抵抗素或脂联素的浓度。结论：这些数据支持以下假设：2型糖尿病患者胰岛素抵抗后代的骨骼肌中的胰岛素抵抗与细胞内脂肪酸代谢异常相关，可能是由于线粒体氧化磷酸化的遗传缺陷。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号