The beta cell in NIDDM: giving light to the blind

Diabetologia. 1994 Sep;37 Suppl 2:S36-42. doi: 10.1007/BF00400824.

Abstract

Impairment of glucose-induced insulin secretion in non-insulin-dependent diabetes mellitus (NIDDM) may be caused by GLUT 2 underexpression in the pancreatic beta cell, a mutation of the glucokinase gene, glucose 6-phosphatase overactivity, FAD-linked glycerophosphate dehydrogenase deficiency, a mitochondrial DNA defect and/or a secondary phenomenon of so-called glucotoxicity possibly involving glycogen accumulation in the beta-cell. It is proposed tht the methyl esters of succinic acid and related molecules may represent new tools with which to bypass these defects in glucose transport, phosphorylation and further catabolism and, hence, to stimulate both proinsulin biosynthesis and insulin release in NIDDM.

Publication types

  • Biography
  • Historical Article
  • Portrait
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Awards and Prizes*
  • Belgium
  • DNA, Mitochondrial / genetics
  • Diabetes Mellitus* / history
  • Diabetes Mellitus, Type 2 / genetics
  • Diabetes Mellitus, Type 2 / physiopathology*
  • Europe
  • Gene Expression
  • Glucose / metabolism
  • Glucose / pharmacology
  • Glucose Transporter Type 2
  • Glycerolphosphate Dehydrogenase / deficiency
  • History, 20th Century
  • Humans
  • Islets of Langerhans / metabolism
  • Islets of Langerhans / physiology
  • Islets of Langerhans / physiopathology*
  • Monosaccharide Transport Proteins / biosynthesis
  • Societies, Medical

Substances

  • DNA, Mitochondrial
  • Glucose Transporter Type 2
  • Monosaccharide Transport Proteins
  • Glycerolphosphate Dehydrogenase
  • Glucose

Personal name as subject

  • W J Malaiise