Hepatic and vascular insulin resistance in PI3kinase p85αdeficientmice

磷脂酰肌醇3-激酶(PI3K)p85α基因缺陷的小鼠表现出低血糖，这是由于周围组织对胰岛素的敏感性和葡萄糖摄取增加的结果。我们先前研究了p85α缺陷小鼠和野生型小鼠的肝脏葡萄糖动态平衡。与野生型小鼠相比，p85α缺陷小鼠的糖异生作用明显增强。在这项研究中，我们评估了p85α缺陷小鼠和野生型小鼠原代肝细胞的肝脏葡萄糖产生。与野生型小鼠相比，p85α缺陷小鼠原代肝细胞的肝糖产量并未降低。

Phosphoinositide 3-kinase (PI3K) p85alpha-deficient mice exhibit hypoglycemia as a result of increased insulin sensitivity and glucose uptake in peripheral tissues. We previouslyinvestigated hepatic glucose homeostasis in p85alpha-deficient and wild-type mice. Gluconeogenesis was rather elevated in p85alpha-deficient mice, compared with in wild-type mice. In this study, we evaluated the hepatic glucose production of primary hepatocyte in p85alpha-deficient and wild-type mice. Hepatic glucose production of primary hepatocyte in p85alpha-deficient mice was not decreased compared to that in wild type mice.