In situ glucose uptake and glucokinase activity of pancreatic islets in diabetic and obese rodents
Autor: | Ying-Jian Wu, Susan Bonner-Weir, S. Efrat, C. D. Berdanier, Franz M. Matschinsky, D. K. Berner, Yin Liang |
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Rok vydání: | 1994 |
Předmět: |
Blood Glucose
Male medicine.medical_specialty endocrine system endocrine system diseases medicine.medical_treatment Glucose uptake Mice Transgenic Diabetes Mellitus Experimental Rats Sprague-Dawley Islets of Langerhans Mice Internal medicine Diabetes mellitus Glucokinase Insulin Secretion medicine Animals Insulin Obesity geography geography.geographical_feature_category Chemistry Pancreatic islets Glucose transporter General Medicine medicine.disease Islet Rats Rats Zucker Mice Inbred C57BL Endocrinology medicine.anatomical_structure Glucose Basal (medicine) Female Research Article |
Zdroj: | The Journal of clinical investigation. 93(6) |
ISSN: | 0021-9738 |
Popis: | The present study evaluated the involvement of glucose transport and phosphorylation in glucose-stimulated insulin release from pancreatic islets. Using quantitative histochemical techniques, we investigated basal islet glucose content, islet glucose uptake in situ during acute extreme experimental hyperglycemia, and islet glucokinase activity in several animal models of diabetes and obesity. The basal islet glucose content in anaesthetized diabetic or obese rodents was either the same or higher than that in their relevant controls. The rate of glucose uptake of islet tissue in these animals after an i.v. glucose injection was different. The db+/db+ mouse and the obese Zucker rat exhibited significantly reduced islet glucose uptake rates. RIP-cHras transgenic mice, BHE/cdb rats and partially pancreatectomized rats showed normal islet glucose uptake rates. The activity of islet glucokinase was increased to a different degree related to the blood glucose level. All five animal models of diabetes or obesity exhibited either a delay or a reduction of insulin release in response to supra maximal glucose stimulation. Our results indicate that the impairment of glucose-induced insulin release in diabetes is not consistently associated with a reduction of islet glucose uptake nor a change of glucokinase activity. |
Databáze: | OpenAIRE |
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