Journal
ACTA BIOCHIMICA ET BIOPHYSICA SINICA
Volume 45, Issue 1, Pages 36-43Publisher
OXFORD UNIV PRESS
DOI: 10.1093/abbs/gms107
Keywords
insulin secretion; amino acid; congenital hyperinsulinism; glutamate dehydrogenase
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Funding
- NIH from Institute of Diabetes, Obesity and Metabolism (University of Pennsylvania) [U01DK089529, DK53012, DK22122]
- Radioimmunoassay and Islet Cores of the Diabetes Research Center of the University of Pennsylvania, Perelman School of Medicine [DK19525]
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK022122, R37DK022122, R01DK053012, U01DK089529, P30DK019525] Funding Source: NIH RePORTER
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The role of amino acids in the regulation of insulin secretion in pancreatic beta-cells is highlighted in three forms of congenital hyperinsulinism (HI), namely gain-of-function mutations of glutamate dehydrogenase (GDH), loss-of-function mutations of ATP-dependent potassium channels, and a deficiency of short-chain 3-hydroxyacyl-CoA dehydrogenase. Studies on disease mouse models of HI suggest that amino acid oxidation and signaling effects are the major mechanisms of amino acid-stimulated insulin secretion. Amino acid oxidation via GDH produces ATP and triggers insulin secretion. The signaling effect of amino acids amplifies insulin release after beta-cell depolarization and elevation of cytosolic calcium.
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