| Abstract: | 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. |
