Abstract
O-GlcNAc and aging: C. elegans as a genetic model to test O-GlcNAc roles in type II diabetic insulin resistance
Highlights
A growing body of literature implicates the intracellular post-translational carbohydrate modification O-GlcNAc in type II diabetic insulin resistance [2, 4, 12, 13]
An insulin receptor-like mutant allele with reduced signaling induces dauer formation, and this was enhanced by an OGA null mutant which elevated O-GlcNAc [3], and inhibited by an OGT null mutant which reduced O-GlcNAc levels [5]
This is reminiscent of the model in which increased hexosamine flux and elevated O-GlcNAc are linked to type II diabetic insulin resistance in mammals
Summary
A growing body of literature implicates the intracellular post-translational carbohydrate modification O-GlcNAc in type II diabetic insulin resistance [2, 4, 12, 13]. C. elegans has a conserved insulin-like signaling pathway which regulates phenotypes including life span, dauer larvae formation, stress responses, and macronutrient storage.
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