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Non‐insulin‐dependent Diabetes Mellitus and Islet B‐cell Mitochondrial Glycerophosphate Dehydrogenase Deficiency
Author(s) -
Malaisse W.J.
Publication year - 1995
Publication title -
diabetic medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.474
H-Index - 145
eISSN - 1464-5491
pISSN - 0742-3071
DOI - 10.1111/j.1464-5491.1995.tb00527.x
Subject(s) - endocrinology , medicine , islet , diabetes mellitus , insulin , pancreatic islets , enzyme , pathogenesis , biochemistry , biology
A deficient activity of the mitochondrial FAD‐linked glycerophosphate dehydrogenase (m‐GDH) in the pancreatic islet B‐cell may represent a contributing factor in the pathogenesis of non‐insulin‐dependent (Type 2) diabetes. This enzyme controls circulation in the glycerol phosphate shuttle and, hence, plays a key role in the B‐cell glucose‐sensing device. An impaired activity of this enzyme in pancreatic islets was documented in several, but not all, animal models of inherited or acquired non‐insulin‐dependent diabetes. Enzymatic studies conducted in lymphocytes or islets from diabetic patients, as well as a search for possible mutations of the m‐GDH gene, were recently undertaken to extend these observations to human subjects.