Yoshiuchi I, Shingu R, Nakajima H, Hamaguchi T, Horikawa Y, Yamasaki T, Oue T, Ono A, Miyagawa J I, Namba M, Hanafusa T, Matsuzawa Y
Second Department of Internal Medicine, Osaka University Medical School, Suita, Japan.
J Clin Endocrinol Metab. 1998 Mar;83(3):1016-9. doi: 10.1210/jcem.83.3.4659.
Glucose-6-phosphatase (G6Pase) catalyzes the rate-limiting step of gluconeogenesis, and hepatic G6Pase activity is increased in diabetes. We have cloned and analyzed the human G6Pase gene promoter region and identified putative regulatory sequences for insulin, cAMP, glucocorticoid, and hepatocyte nuclear factors. The promoter region of the G6Pase gene was analyzed in 154 noninsulin-dependent diabetes mellitus patients and 90 control subjects by PCR-single strand conformation polymorphism and direct sequencing methods. Polymorphisms were not found in any subjects. The results suggested that in noninsulin-dependent diabetic patients, the major cause of the hepatic glucose overproduction was not attributed to dysregulation of the G6Pase gene due to mutation/polymorphism of its promoter region.
葡萄糖-6-磷酸酶（G6Pase）催化糖异生的限速步骤，糖尿病时肝脏G6Pase活性升高。我们已克隆并分析了人G6Pase基因启动子区域，并确定了胰岛素、环磷酸腺苷（cAMP）、糖皮质激素和肝细胞核因子的假定调控序列。采用聚合酶链反应-单链构象多态性及直接测序方法，对154例非胰岛素依赖型糖尿病患者和90例对照者的G6Pase基因启动子区域进行了分析。未在任何受试者中发现多态性。结果提示，在非胰岛素依赖型糖尿病患者中，肝脏葡萄糖过度生成的主要原因并非其启动子区域的突变/多态性导致G6Pase基因调控异常。
