Effect of acute exercise on glycogen synthase in muscle from obese and diabetic subjects

• Published in: American journal of physiology: endocrinology and metabolism Vol. 302; no. 13; p. E82
• Main Authors: Jensen, Jørgen, Tantiwong, Puntip, Stuenae, Jorid T, Molina-Carrion, Marjorie, DeFronzo, Ralph A, Sakamoto, Kei, Musi, Nicolas
• Format: Journal Article
• Language: English
• Published: Bethesda American Physiological Society 01.07.2012
• Subjects: Diabetes; Exercise; Glucose; Insulin resistance; Obesity; Phosphorylation
• ISSN: 0193-1849; 1522-1555

Insulin stimulates glycogen synthase (GS) through dephosphorylation of serine residues, and this effect is impaired in skeletal muscle from insulin-resistant [obese and type 2 diabetic (T2DM)] subjects. Exercise also increases GS activity, yet it is not known whether the ability of exercise to affect GS is impaired in insulin-resistant subjects. The objective of this study was to examine the effect of acute exercise on GS phosphorylation and enzyme kinetic properties in muscle from insulin-resistant individuals. Lean normal glucose-tolerant (NGT), obese NGT, and obese T2DM subjects performed 40 min of moderate-intensity cycle exercise (70% of Vo...). GS kinetic properties and phosphorylation were measured in vastus lateralis muscle before exercise, immediately after exercise, and 3.5 h postexercise. In lean subjects, GS fractional activity increased twofold after 40 min of exercise, and it remained elevated after the 3.5-h rest period. Importantly, exercise also decreased GS K... for UDP-glucose from ...0.5 to ...0.2 mM. In lean subjects, exercise caused significant dephosphorylation of GS by 50-70% (Ser..., Ser..., and Ser...), and phosphorylation of these sites remained decreased after 3.5 h; Ser... phosphorylation was not regulated by exercise. In obese NGT and T2DM subjects, exercise increased GS fractional activity, decreased K... for UDP-glucose, and decreased GS phosphorylation as effectively as in lean NGT subjects. We conclude that the molecular regulatory process by which exercise promotes glycogen synthesis in muscle is preserved in insulin-resistant subjects. (ProQuest: ... denotes formulae/symbols omitted.)