First Author | Turnbull J | Year | 2013 |
Journal | J Biol Chem | Volume | 288 |
Issue | 48 | Pages | 34627-37 |
PubMed ID | 24142699 | Mgi Jnum | J:204966 |
Mgi Id | MGI:5543825 | Doi | 10.1074/jbc.M113.483198 |
Citation | Turnbull J, et al. (2013) Deficiency of a glycogen synthase-associated protein, Epm2aip1, causes decreased glycogen synthesis and hepatic insulin resistance. J Biol Chem 288(48):34627-37 |
abstractText | 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. |