Deficient activity of FAD-linked glycerophosphate dehydrogenase in islets of GK rats

In pancreatic islet extracts of rats with hereditary non-insulin-dependent diabetes mellitus (GK rats), the activity of the mitochondrial FAD-linked glycerophosphate dehydrogenase, as measured by either a radioisotopic or colorimetric procedure, only represented 30 to 40% of that found in control ra...

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Bibliographic Details
Published in:Diabetologia 1993-08, Vol.36 (8), p.722-726
Main Authors: ÖSTENSON, C.-G, ABDEL-HALIM, S. M, RASSCHAERT, J, MALAISSE-LAGAE, F, MEURIS, S, SENER, A, EFENDIC, S, MALAISSE, W. J
Format: Article
Language:English
Subjects:
Alanine Transaminase - metabolism
Animals
Aspartate Aminotransferases - metabolism
Biological and medical sciences
Blood Glucose - metabolism
Diabetes Mellitus, Type 1 - blood
Diabetes Mellitus, Type 1 - enzymology
Diabetes Mellitus, Type 1 - genetics
Diabetes. Impaired glucose tolerance
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Flavin-Adenine Dinucleotide - metabolism
Glutamate Dehydrogenase - metabolism
Glycerolphosphate Dehydrogenase - deficiency
Glycerolphosphate Dehydrogenase - metabolism
Hexokinase - metabolism
Insulin - blood
Insulin - metabolism
Islets of Langerhans - enzymology
Islets of Langerhans - metabolism
Islets of Langerhans - pathology
Isoenzymes - metabolism
Ketoglutarate Dehydrogenase Complex - metabolism
Kinetics
Liver - enzymology
Medical sciences
Mitochondria - enzymology
Mitochondria, Liver - enzymology
Rats
Rats, Mutant Strains
Rats, Wistar
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Summary:In pancreatic islet extracts of rats with hereditary non-insulin-dependent diabetes mellitus (GK rats), the activity of the mitochondrial FAD-linked glycerophosphate dehydrogenase, as measured by either a radioisotopic or colorimetric procedure, only represented 30 to 40% of that found in control rats. This decrease in enzymic activity was not attributable to any sizeable change in either islet DNA content or the relative contribution of insulin-producing beta cells to total islet mass. It contrasted with a normal activity of other mitochondrial dehydrogenases and hexokinase isoenzymes. It coincided, however, with an increased activity of glutamate-pyruvate transaminase, as already observed in adult rats injected with streptozotocin during the neonatal period. The decreased activity of islet FAD-linked glycerophosphate dehydrogenase also contrasted with an increased activity of the same enzyme in the liver of GK, as compared to control rats. In the light of these findings and recent metabolic data collected in intact islets of GK rats, 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.
ISSN:0012-186X
1432-0428
DOI:10.1007/BF00401142