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Exercise-Driven Improvements in Skeletal Muscle Insulin Sensitivity in Type 2 Diabetes: The Role of AS160 Phosphorylation and Glucose Transport Machinery | ||
| New Approaches in Exercise Physiology | ||
| دوره 7، شماره 13، شهریور 2025 | ||
| نوع مقاله: Research Paper | ||
| شناسه دیجیتال (DOI): 10.22054/nass.2025.90177.1216 | ||
| نویسندگان | ||
| saeed naeimi* 1؛ Mohammad Hatami2؛ Mohammad Keyvan gerdekaneh3 | ||
| 1Department of Exercise Physiology, Islamic Azad University, Borujerd Branch, Borujerd, Iran | ||
| 2گروه تربیت بدنی. دانشگاه ملی مهارت، آموزشکده پسران ملایر | ||
| 3Malayer | ||
| چکیده | ||
| Type 2 diabetes mellitus (T2DM) is marked by skeletal-muscle insulin resistance, where impaired intracellular signaling limits glucose transporter trafficking and reduces glucose uptake. Peer-reviewed experimental and clinical studies were synthesized when they reported resistance exercise protocols and quantified AS160 phosphorylation (e.g., Thr642 and/or Ser588), Akt signaling, GLUT4 abundance/translocation, and glycemic outcomes. Acute bout designs typically used 3–5 sets per exercise at 65–85% of one-repetition maximum (1RM), sampling blood and/or muscle within 0–60 min post-exercise, while training interventions most often prescribed 2–3 sessions per week for 8–10 weeks with progressive overload and post-intervention assessments performed 24–72 h after the final session. Across acute studies, resistance exercise increased phospho-AS160 alongside enhanced upstream Akt signaling during early recovery windows, coinciding with heightened insulin-stimulated glucose uptake in skeletal muscle. Across training studies, repeated resistance exercise improved indices of insulin sensitivity and glycemic control and was frequently accompanied by increased GLUT4 content and improved stimulus-dependent AS160 phosphorylation, although changes in total AS160 expression were less consistent. Between-study variability is explained by differences in diabetes induction/models, muscle fiber type examined, biopsy timing, assay methodology, and dietary control. Resistance exercise engages AS160-centered signaling that supports GLUT4 trafficking and improved muscle glucose handling in T2DM. Future trials should standardize sampling windows, report training dose precisely, and integrate molecular endpoints with clinically meaningful glycemic outcomes. | ||
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