Pancreatic islets from healthy (control) and neonatally streptozocin-induced diabetic (STZ-D) rats, a model for non-insulin-dependent diabetes mellitus, were incubated with 3H2O and 5.5 or 16.7 m M glucose. At 5.5 mM glucose, no detectable [3H]glucose was formed. At 16.7 mM, 2.2 patom · islet−1 · h−1 of 3H was incorporated into glucose by the control islets and 5.4 · patom · islet−1 · h−1 by STZ-D islets. About 75% of the 3H was bound to carbon-2 of the glucose. Glucose utilization was 35.3 pmol · islet−1 · h−1 by the control and 19.0 pmol · islet−1 · h−1 by the STZ-D islets· Therefore, 4.5% of the glucose-6-phosphate formed by the control islets and 15.7% by the STZ-D islets was dephosphorylated. This presumably occurred in the β-cells of the islets catalyzed by glucose-6-phosphatase. An increased glucose cycling, i.e., glucose → glucose-6-phosphate → glucose, in islets of STZ-D rats may contribute to the decreased insulin secretion found in these animals.
Glucose Cycling in Islets From Healthy and Diabetic Rats
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Akhtar Khan, Visvanathan Chandramouli, Claes-Göran Östenson, Hans Löw, Bernard R Landau, Suad Efendić; Glucose Cycling in Islets From Healthy and Diabetic Rats. Diabetes 1 April 1990; 39 (4): 456–459. https://doi.org/10.2337/diab.39.4.456
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