Study of hexose transport, glycerol phosphate shuttle and Krebs cycle in islets of adult rats injected with streptozotocin during the neonatal period

@article{Giroix1992StudyOH,
  title={Study of hexose transport, glycerol phosphate shuttle and Krebs cycle in islets of adult rats injected with streptozotocin during the neonatal period},
  author={M H Giroix and Joanne Rasschaert and Abdullah Sener and Viviane Leclercq-Meyer and Danielle Bailb{\'e} and Bernard Portha and Willy J Malaisse},
  journal={Molecular and Cellular Endocrinology},
  year={1992},
  volume={83},
  pages={95-104}
}
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17 Citations
Highly Influential Citations
1
Background Citations
5
Methods Citations
1
Results Citations
2

17 Citations

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
TLDR
It is proposed 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.
Evidence of enhancement of malate-aspartate shuttle activity in beta cells of streptozotocin-induced non-insulin-dependent diabetic rats.
Deficient activity of FAD-linked glycerophosphate dehydrogenase in islets of GK rats
TLDR
It is proposed that a deficiency of beta-cell FAD-linked glycerophosphate dehydrogenase, the key enzyme of the glycerol phosphate shuttle, may represent a cause of inherited non-insulin-dependent diabetes.
Enzymic and metabolic anomalies in islets of diabetic rats: relationship to B cell mass.
TLDR
It is proposed that an altered circulation in the glycerol phosphate shuttle may play a major role in the impaired process of glucose-stimulated insulin release in this model of noninsulin-dependent diabetes.
Is type 2 diabetes due to a deficiency of FAD-linked glycerophosphate dehydrogenase in pancreatic islets?
TLDR
Reduced activity of m-GDH in T-lymphocytes was recently observed in islet, but not liver, homogenates from rats injected with streptozotocin during the neonatal period and in two models of inherited diabetes, i.e. GK rats anddb/db mice.
The role of islet secretory function in the development of diabetes in the GK Wistar rat
TLDR
It is suggested that abnormalities in islet function are present in 8-week-old diabetic animals although these do not seriously impair glucose-stimulated insulin release from isolated islets, and that deterioration of the secretory response is the consequence of some factor associated with the diabetic condition.
Altered NAD(P)H production in neonatal rat islets resistant to H2O2.
Reduced sensitivity of dihydroxyacetone on ATP-sensitive K+ channels of pancreatic beta cells in GK rats
TLDR
It is suggested that the intracellular site responsible for impaired glucose metabolism in pancreatic beta cells of GK rats is located in the glycerol phosphate shuttle.
Effects of fatty acid oxidation on glucose utilization by isolated hepatocytes
Glucose Sensitivity of ATP-Sensitive K+ Channels Is Impaired in β-Cells of the GK Rat: A New Genetic Model of NIDDM
TLDR
The results strongly suggest that the step responsible for the metabolic dysfunction of diabetic β-cells is located within the glycolytic pathway before glyceraldehyde-3-phosphate or in the glycerol phosphate shuttle.
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References

SHOWING 1-10 OF 20 REFERENCES
Impairment of Glycerol Phosphate Shuttle in Islets From Rats With Diabetes Induced by Neonatal Streptozocin
TLDR
It is proposed that the preferential impairment of the oxidative and secretory responses of islet cells to D-glucose in this experimental model of diabetes may be at least partly attributable to an altered transfer of reducing equivalents into the mitochondria as mediated by the glycerol phosphate shuttle.
Hexose metabolism in pancreatic islets. Glucose-induced and Ca(2+)-dependent activation of FAD-glycerophosphate dehydrogenase.
TLDR
Findings support the view that, in islets exposed to a high concentration of D-glucose, a Ca(2+)-induced activation of mitochondrial FAD-glycerophosphate dehydrogenase favours the transfer of reducing equivalents by the glycerol phosphate shuttle, and hence accounts, in part at least, for the preferential stimulation of aerobic glycolysis.
Hexose metabolism in pancreatic islets. Feedback control of D-glucose oxidation by functional events.
Hexose metabolism in pancreatic islets stimulation by D-glucose of [2-3H]glycerol detritiation.
Hexose metabolism in pancreatic islets. Participation of Ca2(+)-sensitive 2-ketoglutarate dehydrogenase in the regulation of mitochondrial function.
Decreased glucose-induced insulin release and biosynthesis by islets of rats with non-insulin-dependent diabetes: effect of tissue culture.
TLDR
Islets of rats with NIDD, once removed from the chronic in vivo exposure to diabetic metabolic disorders, can behave as isolated islets of normal rats, at least as far as insulin handling is concerned.
Insulin Production and Glucose Metabolism in Isolated Pancreatic Islets of Rats With NIDDM
TLDR
The relative unresponsiveness to glucose of islets from NIDDM rats is associated with, and perhaps due to, a deficient islet glucose metabolism.
Glucose Insensitivity and Amino-acid Hypersensitivity of Insulin Release in Rats with Non-insulin-dependent Diabetes: A Study with the Perfused Pancreas
TLDR
Non-insulin-dependent diabetes (NIDDM) was obtained in adult rats following a neonatal streptozotocin injection and the ability of the adenylcyclase to generate cAMP in the B-cells of the diabetics was not decreased, suggesting that the Bcell dysfunction in rats with NIDDM involves a block in glucose metabolism in the early steps of glycolysis prior to the triose-phosphate.
Hexose metabolism in pancreatic islets. Regulation of aerobic glycolysis and pyruvate decarboxylation.
The stimulus-secretion coupling of glucose-induced insulin release XLVI. Physiological role of l-glutamine as a fuel for pancreatic islets
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