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
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Biography
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Historical Article
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Portrait
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Awards and Prizes*
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Belgium
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DNA, Mitochondrial / genetics
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Diabetes Mellitus* / history
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Diabetes Mellitus, Type 2 / genetics
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Diabetes Mellitus, Type 2 / physiopathology*
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Europe
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Gene Expression
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Glucose / metabolism
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Glucose / pharmacology
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Glucose Transporter Type 2
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Glycerolphosphate Dehydrogenase / deficiency
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History, 20th Century
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Humans
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Islets of Langerhans / metabolism
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Islets of Langerhans / physiology
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Islets of Langerhans / physiopathology*
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Monosaccharide Transport Proteins / biosynthesis
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Societies, Medical
Substances
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DNA, Mitochondrial
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Glucose Transporter Type 2
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Monosaccharide Transport Proteins
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Glycerolphosphate Dehydrogenase
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Glucose