ArticleThe Journal of biological chemistry2013
Deficiency of a glycogen synthase-associated protein, Epm2aip1, causes decreased glycogen synthesis and hepatic insulin resistance.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 19 citations in OpenAlex.
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- The admixed brushtail possum genome reveals invasion history in New Zealand and novel imprinted genes.Nature communications · 2023Article
- Transcriptome analysis of peripheral blood mononuclear cells in patients with type 1 diabetes mellitus.Endocrine · 2022Article
- WGCNA-Based DNA Methylation Profiling Analysis on Allopurinol-Induced Severe Cutaneous Adverse Reactions: A DNA Methylation Signature for Predisposing Drug Hypersensitivity.Journal of personalized medicine · 2022Article
- The genomics of rapid climatic adaptation and parallel evolution in North American house mice.PLoS genetics · 2021Article
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- Lafora disease: from genotype to phenotype.Journal of genetics · 2018Review
- The dynamic life of the glycogen granule.The Journal of biological chemistry · 2018Review
- Article
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Authors and funding
17 authors at 2 institutions in 1 country.
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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.
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