Zhang T M, Ostenson C G, Malaisse W J
Laboratory of Experimental Medicine, Brussels Free University, Belgium.
Cell Biochem Funct. 1994 Sep;12(3):185-9. doi: 10.1002/cbf.290120306.
Glycogen accumulation in pancreatic islet cells in situations of sustained hyperglycaemia may participate in the phenomenon of so-called B-cell glucotoxicity. Unexpectedly, however, previously little if any glycogen was found in islet cells of non-insulin-dependent diabetic Goto-Kakizaki rats (GK rats). Therefore, the activities of glycogen synthase, glycogen phosphorylase and alpha-amylase were measured in islets of control and GK rats. No significant difference in enzymatic activity was observed between the control and diabetic animals. In the liver, the activity of glycogen synthase appeared even somewhat higher in GK rats than in control animals. It is concluded that the diabetic syndrome in the GK rats does not involve any major anomaly of glycogen synthase and glycogen phosphorylase activity in the liver of these animals, as well as alpha-amylase, in pancreatic islets.
在持续性高血糖情况下,胰岛细胞中糖原积累可能参与所谓的β细胞糖毒性现象。然而,出乎意料的是,此前在非胰岛素依赖型糖尿病Goto-Kakizaki大鼠(GK大鼠)的胰岛细胞中几乎未发现糖原。因此,测定了对照大鼠和GK大鼠胰岛中糖原合酶、糖原磷酸化酶和α-淀粉酶的活性。对照动物和糖尿病动物之间未观察到酶活性的显著差异。在肝脏中,GK大鼠的糖原合酶活性甚至比对照动物略高。得出的结论是,GK大鼠的糖尿病综合征并不涉及这些动物肝脏中糖原合酶和糖原磷酸化酶活性以及胰岛中α-淀粉酶的任何重大异常。