Zaitsev S, Efanova I, Ostenson C G, Efendić S, Berggren P O
Rolf Luft Center for Diabetes Research, Department of Molecular Medicine, Karolinska Institute, Karolinska Hospital, Stockholm, Sweden.
Biochem Biophys Res Commun. 1997 Oct 9;239(1):129-33. doi: 10.1006/bbrc.1997.7441.
The spontaneously diabetic non-obese GK (Goto-Kakizaki) rat exhibits high basal plasma glucose and insulin levels and poor glucose-induced insulin secretion, which makes it a suitable model for non-insulin dependent diabetes mellitus, NIDDM. The aim of this study was to investigate the handling of cytosolic free Ca2+ concentration ([Ca2+]i), the key regulator of insulin secretion, in GK rat single pancreatic islets. For this purpose the influence of high glucose (16.7 mM) and arginine (20 mM) on [Ca2+]i was studied in GK and Wistar rat islets, which served as controls. The data obtained suggest that glucose which through its metabolism generates ATP needed for closure of the KATP channels and membrane depolarization, induces a delayed [Ca2+]i response in the GK rat pancreatic islet. This delay in [Ca2+]i response is likely to result from a defective metabolism of glucose in the diabetic islet.
自发性糖尿病非肥胖GK（Goto-Kakizaki）大鼠表现出较高的基础血浆葡萄糖和胰岛素水平，以及较差的葡萄糖诱导的胰岛素分泌，这使其成为非胰岛素依赖型糖尿病（NIDDM）的合适模型。本研究的目的是研究GK大鼠单个胰岛中细胞溶质游离钙离子浓度（[Ca2+]i）（胰岛素分泌的关键调节因子）的处理情况。为此，研究了高葡萄糖（16.7 mM）和精氨酸（20 mM）对GK和作为对照的Wistar大鼠胰岛中[Ca2+]i的影响。获得的数据表明，葡萄糖通过其代谢产生关闭KATP通道和膜去极化所需的ATP，在GK大鼠胰岛中诱导延迟的[Ca2+]i反应。这种[Ca2+]i反应延迟可能是由于糖尿病胰岛中葡萄糖代谢缺陷所致。
