PINITOL SUPPLEMENTATION NOT AFFECT INSULIN-MEDIATED GLUCOSE METABOLISM AND

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。补充松醇不影响老年人胰岛素介导的葡萄糖代谢和肌肉胰岛素受体含量和磷酸化：本研究评估了口服补充松醇对口服和静脉葡萄糖耐量以及对老年人骨骼肌胰岛素受体含量和磷酸化的影响。15人（6名男性，9名女性;年龄66 <$8岁; BMI 27.9 <$3.3 kg/m2;血红蛋白A1 c 5.39 <$0.46%，平均<$SD）完成了7周方案。受试者被随机分配到在第2-7周期间每天消耗两次非营养性饮料（安慰剂组，n = 8）或溶解有1000 mg松醇的相同饮料（松醇组，n = 7，总剂量= 2000 mg松醇/d）的组中。在第1周和第7周进行检测。在补充Pinitol组中，24小时尿Pinitol排泄量增加了17倍。葡萄糖、胰岛素和C肽的空腹浓度以及这些化合物在口服（75 g）和静脉内（300 mg/kg）葡萄糖耐量挑战中的180 min曲线下面积从第1周至第7周没有变化，也没有受到松醇的影响。此外，松醇不影响指数的肝脏和全身胰岛素敏感性从口服葡萄糖耐量试验和指数的胰岛素敏感性，急性胰岛素对葡萄糖的反应，和葡萄糖的有效性从静脉内葡萄糖耐量试验，估计使用最小建模。在口服葡萄糖诱导的高血糖和高胰岛素血症状态下采集的股外侧肌样本中，Pinitol对总胰岛素受体含量和胰岛素受体磷酸酪氨酸1158和胰岛素受体磷酸酪氨酸1162/1163活化没有差异性影响。这些数据表明，补充松醇不影响全身胰岛素介导的葡萄糖代谢和肌肉胰岛素受体含量和磷酸化在非糖尿病，老年人。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Pinitol Supplementation Does Not Affect Insulin-Mediated Glucose Metabolism and Muscle Insulin Receptor Content and Phosphorylation in Older Humans: This study assessed the effect of oral pinitol supplementation on oral and intravenous glucose tolerances and on skeletal muscle insulin receptor content and phosphorylation in older people. Fifteen people (6 men, 9 women; age 66 ¿ 8 y; BMI 27.9 ¿ 3.3 kg/m2; hemoglobin A1c 5.39 ¿ 0.46%, mean ¿ SD) completed a 7-wk protocol. Subjects were randomly assigned to groups that during wk 2-7 consumed twice daily either a non-nutritive beverage (Placebo group, n = 8) or the same beverage with 1000 mg pinitol dissolved into it (Pinitol group, n = 7, total dose = 2000 mg pinitol/d). Testing was done at wk 1 and wk 7. In the Pinitol group with supplementation, 24-h urinary pinitol excretion increased 17-fold. The fasting concentrations of glucose, insulin, and C-peptide, and the 180-min area under the curve for these compounds, in response to oral (75 g) and intravenous (300 mg/kg) glucose tolerance challenges, were unchanged from wk 1 to wk 7 and were not influenced by pinitol. Also, pinitol did not affect indices of hepatic and whole-body insulin sensitivity from the oral glucose tolerance test and indices of insulin sensitivity, acute insulin response to glucose, and glucose effectiveness from the intravenous glucose tolerance test, estimated using minimal modeling. Pinitol did not differentially affect total insulin receptor content and insulin receptor phosphotyrosine 1158 and insulin receptor phosphotyrosine 1162/1163 activation in vastus lateralis samples taken during an oral-glucose-induced hyperglycemic and hyperinsulinemic state. These data suggest that pinitol supplementation does not influence whole-body insulin-mediated glucose metabolism and muscle insulin receptor content and phosphorylation in nondiabetic, older people.