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

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Type 2 diabetic patients exhibit reduced insulin-stimulated glucose disposal
rates 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.
Original languageEnglish
JournalDiabetes Management
Pages (from-to)81-90
Number of pages10
Publication statusPublished - 2013

    Research areas

  • Faculty of Science - Type 2 diabetes, Physiological aspects, Muscles, Glycogen

ID: 273698731