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Abstract

Click to add/remove this article to your list of 'My Favorites' Acute and Chronic Exercise Regulate AMP-Activated Protein Kinase in Rat Adipocytes

Year: 2005

Abstract Number: 59-OR

Authors: HO-JIN KOH, NAOKO MUKAI, YASUKO MANABE, RICHARD C. HO, NOBUHARU FUJII, MICHAEL F. HIRSHMAN, LAURIE J. GOODYEAR

Institutions: Boston, MA

Results: An acute bout of exercise increases lipolysis in fat cells, and chronic exercise training reduces fat cell size, presumably by repeated activation of the lipolytic process. Recent evidence suggests that AMPK is a positive regulator of lipolysis in 3T3-L1 adipocytes, therefore we studied AMPK signaling in rat parametrial fat cells in response to both acute and chronic exercise. Female SD rats exercised on a treadmill at 20 m/min, 12% grade for 15, 30, or 60 min, or for 60 min and studied 1 hr post (n=5/group). Both AMPKa1 and a2 activities were significantly increased 2-3 fold with 15 and 30 min exercise, but were not increased with 60 min exercise or at 1 hr post. The increases were paralleled by increased phosphorylation of the regulatory Thr172 site of AMPK and Ser79 of ACC, a downstream AMPK substrate. These experiments show that acute exercise results in a rapid, but transient activation of both AMPK catalytic isoforms. For the training study, 12 rats served as sedentary controls and 10 rats exercised for 8 wks, running 120 min/day, 32 m/min, 15% grade for the last 2 wks. Rats were studied in the basal state, 36 hr after the last training session. Training significantly decreased parametrial fat mass (2.4±0.2 vs. 1.2±0.1 g) and serum leptin (0.7±0.1 vs. 0.4±0.1 ng/ml), and dramatically increased serum adiponectin (2.2±0.4 vs. 5.8±0.8 μg/ml). Training profoundly altered fat cells, significantly increasing AMPKα1 activity (2.3-fold) and protein expression (1.4-fold), AMPKα2 activity (1.9-fold) and protein (3.3-fold), AMPK phosphorylation (1.4-fold), ACC phosphorylation (2-fold) and protein (2.7-fold), and expression of an AMPK kinase, LKB1 (2.2-fold). These data suggest that the increased AMPK activity with chronic exercise may be due to the combination of increased serum adiponectin and expression of AMPK and LKB1. In conclusion, AMPK kinase is robustly regulated by both acute and chronic exercise in rat fat cells and therefore, is likely to play an important role in the regulation of fatty acid metabolism in this tissue.

Category: Exercise - Animal