AMP‐activated protein kinase response to aerobic exercise training prevents glucose intolerance induced by hypercaloric diet

Abstract

Hypercaloric diet (cafeteria) is known to induce glucose intolerance (GI). We investigated whether exercise training (ET) would prevent GI and the role of AMP-activated protein kinase (AMPK)/acetyl CoA carboxylase (ACC) pathway behind this response. Male C57BL/6J mice were assigned into chow-fed controls (C, n=5), cafeteria diet (CAF, n=5), chow-fed trained (TR, n=8), and cafeteria diet plus trained (CAF-TR, n=8). ET was performed simultaneously with diet and consisted of 8-wk running session of 60 min, 5 days/wk. Intraperitoneal Glucose Tolerance Test (GTT) was performed before and after ET. Exercise tolerance was determined by graded treadmill test, body weight (BW), fat pads weight (retroperitoneal and epididymal) and insulin level were measured. Expression of AMPK, AMPK phosphorylation at á-Thr172 (P-AMPK), ACC and ACC phosphorylation at Ser 79 (P-ACC) in skeletal muscle were determined by Western blot. After ET, TR and CAF-TR increased exercise tolerance, reduced BW (p<0.05) but fat pads weight decreased only in TR (p<0.05). Plasma glucose and insulin did not change. Before ET, all groups showed similar response in GTT, but after dietary treatment CAF showed GI during GTT (p<0.05), which was counteracted by ET in CAF-TR. AMPK, P-AMPK, ACC and P-ACC increased in CAF-TR (p<0.05). In conclusion, cafeteria diet is associated with GI development and ET prevents this response by activating the AMPK/ACC pathway.