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FAD‐linked glycerophosphate dehydrogenase deficiency in pancreatic islets of mice with hereditary diabetes
Author(s) -
Sener Abdullah,
Herberg Lieselotte,
Malaisse Willy J.
Publication year - 1993
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(93)81297-d
Subject(s) - endocrinology , medicine , islet , dehydrogenase , glutamate dehydrogenase , diabetes mellitus , pancreatic islets , pathogenesis , enzyme , insulin , biology , chemistry , biochemistry , glutamate receptor , receptor
The mitochondrial enzyme FAD‐linked glycerophosphate dehydrogenase plays a key role in the glucose‐sensing device of the insulin‐producing pancreatic B‐cell. Its activity was found to be decreased in islet, but not liver, homogenates of BL/Ks‐ db/db mice, in which diabetes mellitus represents an inherited disease. The decreased activity of FAD‐linked glycerophosphate dehydrogenase contrasted with a normal activity of glutamate dehydrogenase and 2‐ketoglutarate dehydrogenase in the islets of db/db mice. It is proposed that a site‐specific defect of FAD‐linked glycerophosphate dehydrogenase in the pancreatic B‐cell might represent a far‐from‐uncommon causal or contributing factor in the pathogenesis of non‐insulin‐dependent diabetes mellitus.