AMP-activated protein kinase regulates the expression of monocarboxylate transporter 4 in skeletal muscle

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• 作者：Ayako Furugen^a ; Masaki Kobayashi^a ; Katsuya Narumi^a ; Meguho Watanabe^a ; Sho Otake^a ; Shirou Itagaki^a ; Ken Iseki ; ^a ; ^{ken-i@pharm.hokudai.ac.jp}
• 关键词：AMPK ; MCT4 ; Up-regulation ; L-lactic acid ; Skeletal muscle
• 刊名：Life Sciences
• 出版年：2011
• 出版时间：17 January 2011
• 年：2011
• 卷：88
• 期：3-4
• 页码：163-168
• 全文大小：536 K

文摘

Aims

The aim of this study was to determine the effect of 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR), an AMP-activated protein kinase (AMPK) activator, on monocarboxylate transporter 4 (MCT4) expression in rat skeletal muscle and a prototypic embryonal rhabdomyosarcoma cell line (RD cells).

Main methods

We examined the alteration in Glucose transporter 4 (GLUT4) and MCT4 mRNA levels by quantitative real-time PCR. Alteration in GLUT4 and MCT4 protein levels was examined by Western blotting.

Key findings

In an in vivo study, AICAR increased MCT4 mRNA and protein levels in a fiber-type specific manner. In an in vitro study, AICAR increased MCT4 mRNA and protein levels. Moreover, AICAR-induced MCT4 expression was blocked by Compound C, an AMPK inhibitor.

Significance

In this study, we found that AMPK activation induced expression of MCT4 in RD cells and rat skeletal muscle in a fiber-type specific manner. These results indicate the possible involvement of an AMPK-mediated pathway associated with MCT4 expression in skeletal muscle.