Ishihara H, Tashiro F, Ikuta K, Asano T, Katagiri H, Inukai K, Kikuchi M, Yazaki Y, Oka Y, Miyazaki J
Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
FEBS Lett. 1995 Sep 11;371(3):329-32. doi: 10.1016/0014-5793(95)00932-y.
We have generated transgenic mice, in either C57BL/6 or C3H background, expressing antisense glucokinase mRNA in beta-cells. The glucose phosphorylating activity at 60 mM glucose in transgenic islets was significantly lower than that in controls, and the insulin secretory response to glucose was lower in transgenic islets than in those of controls in both strains. Following i.p. glucose challenge, higher blood glucose levels were observed in transgenic mice than in controls in the C57BL/6 but not the C3H background. These data suggest that a beta-cell secretory defect, in combination with other undefined genetic factors, causes impaired glucose homeostasis in mice.
我们已经培育出了在C57BL/6或C3H背景下的转基因小鼠，这些小鼠的β细胞中表达反义葡萄糖激酶mRNA。转基因胰岛在60 mM葡萄糖浓度下的葡萄糖磷酸化活性显著低于对照组，并且在这两种品系中，转基因胰岛对葡萄糖的胰岛素分泌反应均低于对照组。腹腔注射葡萄糖刺激后，在C57BL/6背景而非C3H背景下，观察到转基因小鼠的血糖水平高于对照组。这些数据表明，β细胞分泌缺陷与其他未明确的遗传因素共同导致了小鼠葡萄糖稳态受损。
