Regulation of glycogen synthase in muscle and its role in Type 2 diabetes

Publikation: Bidrag til tidsskriftReviewfagfællebedømt

Standard

Regulation of glycogen synthase in muscle and its role in Type 2 diabetes. / Kleinert, Maximilian; Sylow, Lykke; Richter, Erik A.

I: Diabetes Management, 2013, s. 81-90.

Publikation: Bidrag til tidsskriftReviewfagfællebedømt

Harvard

Kleinert, M, Sylow, L & Richter, EA 2013, 'Regulation of glycogen synthase in muscle and its role in Type 2 diabetes', Diabetes Management, s. 81-90. https://doi.org/10.2217/dmt.12.54

APA

Kleinert, M., Sylow, L., & Richter, E. A. (2013). Regulation of glycogen synthase in muscle and its role in Type 2 diabetes. Diabetes Management, 81-90. https://doi.org/10.2217/dmt.12.54

Vancouver

Kleinert M, Sylow L, Richter EA. Regulation of glycogen synthase in muscle and its role in Type 2 diabetes. Diabetes Management. 2013;81-90. https://doi.org/10.2217/dmt.12.54

Author

Kleinert, Maximilian ; Sylow, Lykke ; Richter, Erik A. / Regulation of glycogen synthase in muscle and its role in Type 2 diabetes. I: Diabetes Management. 2013 ; s. 81-90.

Bibtex

@article{a3f3fb5bf9cf43e1b782acddb33427c7,
title = "Regulation of glycogen synthase in muscle and its role in Type 2 diabetes",
abstract = "Type 2 diabetic patients exhibit reduced insulin-stimulated glucose disposalrates along with impaired muscle glycogen synthase (GS) activity and glycogen synthesis. After a meal, muscle is an important glucose sink and a large proportion of glucose entering muscle is converted to glycogen. It is, therefore, a clinically relevant question to ask whether impaired GS activation and glycogen storage in muscle are defects responsible for reduced glucose disposal in Type 2 diabetes. This short review first provides a brief mechanistic background on regulation of GS activity and then presents evidence from human and rodent studies to discuss the possible role of dysregulated GS in the etiology of Type 2 diabetes. We conclude that impaired GS activity and glycogen synthesis in skeletal muscle of Type 2 diabetic patients is mainly a secondary manifestation of skeletal muscle insulin resistance of glucose transport.",
keywords = "Faculty of Science, Type 2 diabetes, Physiological aspects, Muscles, Glycogen",
author = "Maximilian Kleinert and Lykke Sylow and Richter, {Erik A.}",
note = "CURIS 2013 NEXS 364",
year = "2013",
doi = "10.2217/dmt.12.54",
language = "English",
pages = "81--90",
journal = "Diabetes Management",
issn = "1758-1907",
publisher = "Future Medicine Ltd.",

}

RIS

TY - JOUR

T1 - Regulation of glycogen synthase in muscle and its role in Type 2 diabetes

AU - Kleinert, Maximilian

AU - Sylow, Lykke

AU - Richter, Erik A.

N1 - CURIS 2013 NEXS 364

PY - 2013

Y1 - 2013

N2 - Type 2 diabetic patients exhibit reduced insulin-stimulated glucose disposalrates along with impaired muscle glycogen synthase (GS) activity and glycogen synthesis. After a meal, muscle is an important glucose sink and a large proportion of glucose entering muscle is converted to glycogen. It is, therefore, a clinically relevant question to ask whether impaired GS activation and glycogen storage in muscle are defects responsible for reduced glucose disposal in Type 2 diabetes. This short review first provides a brief mechanistic background on regulation of GS activity and then presents evidence from human and rodent studies to discuss the possible role of dysregulated GS in the etiology of Type 2 diabetes. We conclude that impaired GS activity and glycogen synthesis in skeletal muscle of Type 2 diabetic patients is mainly a secondary manifestation of skeletal muscle insulin resistance of glucose transport.

AB - Type 2 diabetic patients exhibit reduced insulin-stimulated glucose disposalrates along with impaired muscle glycogen synthase (GS) activity and glycogen synthesis. After a meal, muscle is an important glucose sink and a large proportion of glucose entering muscle is converted to glycogen. It is, therefore, a clinically relevant question to ask whether impaired GS activation and glycogen storage in muscle are defects responsible for reduced glucose disposal in Type 2 diabetes. This short review first provides a brief mechanistic background on regulation of GS activity and then presents evidence from human and rodent studies to discuss the possible role of dysregulated GS in the etiology of Type 2 diabetes. We conclude that impaired GS activity and glycogen synthesis in skeletal muscle of Type 2 diabetic patients is mainly a secondary manifestation of skeletal muscle insulin resistance of glucose transport.

KW - Faculty of Science

KW - Type 2 diabetes

KW - Physiological aspects

KW - Muscles

KW - Glycogen

UR - http://www.futuremedicine.com/doi/abs/10.2217/dmt.12.54

U2 - 10.2217/dmt.12.54

DO - 10.2217/dmt.12.54

M3 - Review

SP - 81

EP - 90

JO - Diabetes Management

JF - Diabetes Management

SN - 1758-1907

ER -

ID: 273698731