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J. Biol. Chem., Vol. 281, Issue 22, 99917, June 2, 2006

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Sweetly Controlling Glutamate Oxidation

Congenital hyperinsulinism (HI) is a group of disorders that cause hypoglycemia in infants and children. The majority of these cases appears to be due to genetic defects in the regulation of insulin secretion by pancreatic -cells. For example, children with mutations in glutamate dehydrogenase (GDH) experience a hyperinsulinism-hyperammonemia syndrome (GDH-HI), and their -cells are sensitized to leucine stimulation.

To increase understanding of the role of GDH in insulin secretion, Changhong Li and colleagues generated GDH transgenic mice that expressed in islets the mutant human GDH-HI H454Y and human wild-type GDH with the rat insulin promoter. The H454Y GDH transgenic mice had hypoglycemia, confirming that the H454Y mutation can cause disease. Enhancement of insulin release by the H454Y GDH mutation or by leucine activation was associated with increased oxidative deamination of glutamate via GDH. These results confirm that in mouse islets GDH functions predominantly in the direction of glutamate oxidation rather than glutamate synthesis, and this flux is tightly controlled by glucose.

FOOTNOTES

See referenced article, J. Biol. Chem. 2006, 281, 15064–15072

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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Related Collections Papers Of The Week Social Bookmarking                      What's this?