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Glucose Metabolism in Goto-Kakizaki Rat Islets¹

Department of Molecular Medicine, Endocrine and Diabetes Unit, Rolf Luft Center for Diabetes Research, Karolinska Hospital, S-171 76 Stockholm; and the Department of Clinical Chemistry, Huddinge University Hospital, S-141 86 Huddinge, Sweden; and the Departments of Medicine and Biochemistry, Case Western Reserve University, Cleveland, Ohio 44106

Islets from Goto-Kakizaki (GK) rats from our colony, despite marked impairment of glucose-induced insulin release, used glucose and produced CO₂ at a rate 3 times that of islets from control Wistar rats. Almost all glucose used was accounted for in CO₂ and lactate production. The percentages of glucose carbon used collected in CO₂ and lactate were similar for control and GK islets. GK islets also oxidized 40% more acetate and leucine to CO₂ than did control islets. The fraction of carbon leaving the Krebs cycle relative to CO₂ production was the same in GK and control islets. The capacities of mitochondria from GK islets to generate ATP from glutamate and malate were similar and that to generate ATP from succinate and rotenone was somewhat less from GK islets. The reason for the enhanced utilization of substrates by islets of the GK rat is not apparent. In conclusion, there is no decrease in islet glucose utilization, glucose oxidation, Krebs cycle function, or the electron transport system evident from these measurements to explain the impaired insulin release in islets from GK rats.

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