ArticleDiabetologia1993
Preferential alteration of oxidative relative to total glycolysis in pancreatic islets of two rat models of inherited or acquired type 2 (non-insulin-dependent) diabetes mellitus.
Article in Diabetologia, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- Article
- A high carbohydrate diet does not induce hyperglycaemia in a mitochondrial glycerol-3-phosphate dehydrogenase-deficient mouse.Diabetologia · 2003Article
- The role of islet secretory function in the development of diabetes in the GK Wistar rat.Diabetologia · 1994Article
- Metabolism of endogenous nutrients in islets of Goto-Kakizaki (GK) rats.The Biochemical journal · 1993Article
- Deficient activity of FAD-linked glycerophosphate dehydrogenase in islets of GK rats.Diabetologia · 1993Article
- Is type 2 diabetes due to a deficiency of FAD-linked glycerophosphate dehydrogenase in pancreatic islets?Acta diabetologica · 1993Review
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
In islets from both adult rats injected with streptozotocin during the neonatal period and spontaneously diabetic rats obtained by repeated selective breedings (GK rats), the ratio between D-[3,4-14C]glucose oxidation and D-[5-3H]glucose conversion to 3HOH was 25% lower than in islets from control rats, indicating an impaired contribution of oxidative to total glycolysis. No primary defect in the Krebs cycle was found in the islets of diabetic rats, as judged from the ratio between either D-[2-14C]glucose or D-[6-14C]glucose and D-[3,4-14C]glucose oxidation. Therefore, we propose that a preferential alteration of oxidative glycolysis in the pancreatic beta cell may contribute to the impairment of glucose-induced insulin release not only in a cytotoxic but also in a spontaneous model of non-insulin-dependent diabetes mellitus.
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