Non-insulin-dependent diabetes mellitus and islet B-cell mitochondrial glycerophosphate dehydrogenase deficiency.
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.
Malaisse
W J
WJ
Laboratory of Experimental Medicine, Brussels Free University, Belgium.
D003924:Diabetes Mellitus, Type 2 / Q000201:enzymology*; D005993:Glycerolphosphate Dehydrogenase / Q000172:deficiency*; D006801:Humans; D007515:Islets of Langerhans / Q000201:enzymology* / Q000648:ultrastructure; D008928:Mitochondria / Q000201:enzymology*
D005993:Glycerolphosphate Dehydrogenase