Long-term exercise stimulates adenosine monophosphate-activated protein kinase activity and subunit expression in rat visceral adipose tissue and liver

Adenosine monophosphate-activated protein kinase (AMPK) is activated in response to adenosine triphosphate depletion caused by the metabolic and nutritional state. Mammalian AMPK is a heterotrimeric enzyme composed of a catalytic α subunit and 2 regulatory subunits (β and γ). Although much attention has been focused on exercise-induced AMPK activation in skeletal muscle, little information is available on the role of AMPK in adipose tissue and liver. Acetyl-coenzyme A carboxylase (ACC) is a well-known downstream target of AMPK. The ACC contains serine residues that are phosphorylated by AMPK. The present study was undertaken to determine whether long-term exercise of medium intensity (60% of V˙o2max for 12 weeks) may influence AMPK enzyme activity, gene/protein expression, and subsequent ACC phosphorylation in rat adipose tissue (visceral and subcutaneous) and liver. We initially demonstrated that long-term exercise induced a significant increase in phosphorylation of Thr172 in the AMPK α1 subunit and of Ser79 in ACC in visceral adipose tissue rather than subcutaneous tissue. We also demonstrated that the AMPK α1-,α2-subunit messenger RNA (mRNA) level as well as the corresponding protein levels were increased in response to long-term exercise, whereas the other subunits were not altered significantly. In contrast to that of visceral adipose tissue, long-term exercise did not induce any significant effect on any of the AMPK subunit mRNA levels or α1-,α2-subunit protein levels in subcutaneous adipose tissue. In addition to adipose tissue, we demonstrated that long-term exercise induced an increase in both AMPK/ACC phosphorylation and α1-,α2-subunit mRNA/protein expression in the liver. Although the precise physiologic relevance of AMPK activation in these tissues remains unknown, it is possible that it might play an important role in long-term exercise-induced adaptation mechanisms and may lead to an improvement in certain metabolic abnormalities in metabolic diseases.