Regulation of glycogen synthase in muscle and its role in Type 2 diabetes
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Regulation of glycogen synthase in muscle and its role in Type 2 diabetes. / Kleinert, Maximilian; Sylow, Lykke; Richter, Erik A.
In: Diabetes Management, 2013, p. 81-90.Research output: Contribution to journal › Review › Research › peer-review
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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