Department of Pathology and Laboratory Medicine, Children's Hospital of Philadelphia Research Institute, Philadelphia, PA, United States.
FEBS Lett. 2011 May 6;585(9):1345-9. doi: 10.1016/j.febslet.2011.04.005. Epub 2011 Apr 7.
The recent creation of the PANDER (pancreatic-derived factor) knockout (PANKO) and acute mouse models have revealed a biological function in the regulation of glycemic levels via promotion of hepatic glucose production (HGP) and pancreatic β-cell insulin secretion. Therefore, we hypothesized that the absence of PANDER may afford some degree of protection from high-fat diet (HFD) induced fasting hyperglycemia. On HFD, fasting glycemic levels were significantly lower in the PANKO mice. Also, fasting insulin levels and the in vivo insulin response following glucose injection were inhibited in PANKO mice. The lowered fasting glycemic levels are attributed to decreased HGP due to the absence of PANDER. Overall, our findings further indicate PANDER impacts glycemic levels and may represent a potential but complicated therapeutic target.
最近创建的 PANDER（胰腺衍生因子）敲除（PANKO）和急性小鼠模型揭示了其在通过促进肝葡萄糖生成（HGP）和胰腺β细胞胰岛素分泌来调节血糖水平方面的生物学功能。因此，我们假设 PANDER 的缺失可能在一定程度上提供了对高脂肪饮食（HFD）诱导的空腹高血糖的保护作用。在 HFD 喂养下，PANKO 小鼠的空腹血糖水平显著降低。此外，PANKO 小鼠的空腹胰岛素水平和葡萄糖注射后的体内胰岛素反应受到抑制。由于缺乏 PANDER，空腹血糖水平降低归因于 HGP 的减少。总的来说，我们的研究结果进一步表明 PANDER 影响血糖水平，并可能代表一个潜在但复杂的治疗靶点。
