PINITOL SUPPLEMENTATION NOT AFFECT INSULIN-MEDIATED GLUCOSE METABOLISM AND

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。补充匹尼醇不会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：本研究评估了口服匹尼醇补充对老年人口服和静脉葡萄糖耐量以及骨骼肌胰岛素受体含量和磷酸化的影响。15人（6男9女，年龄66±8岁，BMI 27.9±3.3 kg/m2，血红蛋白A1c 5.39±0.46%,mean¿SD）完成了7周的方案。受试者被随机分为两组，在第2-7周每天饮用两次无营养饮料（安慰剂组，n = 8）或含有1000 mg匹尼托醇的相同饮料（匹尼托醇组，n = 7，总剂量= 2000 mg匹尼托醇/d）。在第1周和第7周进行测试。在补充匹尼醇组，24小时尿匹尼醇排泄量增加17倍。在口服（75 g）和静脉注射（300 mg/kg）葡萄糖耐量挑战下，葡萄糖、胰岛素和c肽的空腹浓度以及这些化合物在曲线下的180分钟面积从第1周到第7周保持不变，不受匹尼醇的影响。此外，pinitol不影响口服糖耐量试验的肝脏和全身胰岛素敏感性指标，也不影响静脉糖耐量试验的胰岛素敏感性、急性胰岛素对葡萄糖的反应和葡萄糖有效性指标，这些指标使用最小模型进行估计。在口服葡萄糖诱导的高血糖和高胰岛素状态下，匹尼醇对股外侧肌样本的总胰岛素受体含量、胰岛素受体磷酸酪氨酸1158和胰岛素受体磷酸酪氨酸1162/1163的激活没有差异。这些数据表明，补充匹尼醇不会影响非糖尿病老年人的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。

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.