Abstract
Glycogen synthesis is a major component of the insulin response, and defective glycogen synthesis is a major portion of insulin resistance. Insulin regulates glycogen synthase (GS) through incompletely defined pathways that activate the enzyme through dephosphorylation and, more potently, allosteric activation. We identify Epm2aip1 as a GS-associated protein. We show that the absence of Epm2aip1 in mice impairs allosteric activation of GS by glucose 6-phosphate, decreases hepatic glycogen synthesis, increases liver fat, causes hepatic insulin resistance, and protects against age-related obesity. Our work identifies a novel GS-associated GS activity-modulating component of insulin resistance.
Original language | English (US) |
---|---|
Pages (from-to) | 34627-34637 |
Number of pages | 11 |
Journal | Journal of Biological Chemistry |
Volume | 288 |
Issue number | 48 |
DOIs | |
State | Published - Nov 29 2013 |
ASJC Scopus subject areas
- Biochemistry
- Molecular Biology
- Cell Biology