Abstract
Glycogen is the primary storage form of glucose, which is metabolized actively in the liver and skeletal muscle of mammals. The skeletal muscle glycogen is used intracellularly to provide starting substrate for glycolysis, whereas liver glycogen is used mainly for the maintenance of blood glucose homeostasis. The conversion of glucose to glycogen is an ordered process, in which the enzyme glycogen synthase plays an essential role. The key events in the synthesis of glycogen have been elucidated in both the liver and muscle. The process of understanding the regulatory mechanism of glycogen synthase activity has led to the discoveries of many important players in cellular metabolism. Research in identifying factors modulating muscle glycogen synthesis has been of popular interest within the past decade. The goal of this review is to summarize potential factors affecting skeletal muscle glycogen synthase expression level and activity in literatures published for the past decade.
Highlights
The ability to acquire and store energy is essential for an organism to face environmental challenges such as the lack of readily available nutrients
The activation of insulin signaling pathway increases the activities of enzymes involved in glycogenesis including Glycogen Synthase (GS), and in turn, enhance glycogenesis in hepatocytes and muscle cells [3,4]
A study aimed to elucidate the role of the Glycogen Synthase Kinase (GSK)-3α in insulin resistance of human skeletal muscle cells from non-diabetic subjects found that the reduction of GSK-3α expression resulted in an increase of the insulin-induced glucose uptake and GS fractional velocity
Summary
The ability to acquire and store energy is essential for an organism to face environmental challenges such as the lack of readily available nutrients. Another group who investigated the effects of endurance training on glucose metabolism in skeletal muscle found that in middle-aged males who regularly perform endurance physical activity had significantly higher GS protein levels than that of healthy sedentary controls [34]. A study aimed to elucidate the role of the GSK-3α in insulin resistance of human skeletal muscle cells from non-diabetic subjects found that the reduction of GSK-3α expression resulted in an increase of the insulin-induced glucose uptake and GS fractional velocity.
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