Organizing glucose disposal: emerging roles of the glycogen targeting subunits of protein phosphatase-1.
Abstract
Glucose is stored in mammalian tissues in the form of glycogen. Glycogen levels are markedly reduced in liver or muscle cells of patients with insulin-resistant or insulin-deficient forms of diabetes, suggesting that impaired glycogen synthesis may contribute to development of hyperglycemia. Recently, interest in this area has been further stimulated by new insights into the spatial organization of metabolic enzymes within cells and the importance of such organization in regulation of glycogen metabolism. It is now clear that a four-member family of glycogen targeting subunits of protein phosphatase-1 (PP1) plays a major role in coordinating these events. These proteins target PP1 to the glycogen particle and also bind differentially to glycogen synthase, glycogen phosphorylase, and phosphorylase kinase, thereby serving as molecular scaffolds. Moreover, the various glycogen-targeting subunits have distinct tissue expression patterns and can influence regulation of glycogen metabolism in response to glycogenic and glycogenolytic signals. The purpose of this article is to summarize new insights into the structure, function, regulation, and metabolic effects of the glycogen-targeting subunits of PP1 and to evaluate the possibility that these molecules could serve as therapeutic targets for lowering of blood glucose in diabetes.
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Under anabolic conditions, insulin increases glycogen synthesis by activating glycogen synthase and inhibiting glycogen phosphorylase.
“Under anabolic conditions, insulin augments glycogen synthesis by simultaneously activating glycogen synthase and inhibiting glycogen phosphorylase [148, 149].”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [149]
Glycogen synthase exists in active (dephosphorylated) and inactive (phosphorylated) forms.
“Glycogen synthase exists in an active (dephosphorylated) and an inactive (phosphorylated) form [148–150].”
From Pathogenesis of insulin resistance in skeletal muscle (2010) · cites this paper as [149]
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References 78 · Cited by 189
- Authors
- Newgard, C. B., Brady, M. J., O'Doherty, R. M., & Saltiel, A. R.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2000-12-01
- Volume
- 49
- Issue
- 12
- Pages
- 1967-1977
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2169250745
- Cited by
- 189
- References
- 78
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 5 · 2023: 5 · 2022: 8 · 2021: 7 · 2020: 9 · 2019: 7 · 2018: 4 · 2017: 5 · 2016: 7 · 2015: 15 · 2014: 8 · 2013: 2 · 2012: 3
- FWCI
- 8.31
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (P01DK058398, P01 DK58398)
- Topics
- Health Sciences › Medicine › Rheumatology › Glycogen Storage Diseases and Myoclonus
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- protein phosphatase 1, glycogen metabolism, glycogen synthase, glycogen phosphorylase, phosphorylase kinase, molecular scaffolds, insulin resistance, glucose disposal, therapeutic target
- MeSH terms
- Animals, Diabetes Mellitus, Glucose, Glycogen, Humans, Phosphoprotein Phosphatases, Structure-Activity Relationship, Protein Isoforms, Protein Phosphatase 1
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