A comparison of chronic AICAR treatment-induced metabolic adaptations in red and white muscles of rats

Masataka Suwa, Hiroshi Nakano, Zsolt Radak, Shuzo Kumagai

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

The signaling molecule 5′-AMP-activated protein kinase plays a pivotal role in metabolic adaptations. Treatment with 5-aminoimidazole-4-carboxamide-1-β-d-ribofranoside (AICAR) promotes the expression of metabolic regulators and components involved in glucose uptake, mitochondrial biogenesis, and fatty acid oxidation in skeletal muscle cells. Our aim was to determine whether AICAR-induced changes in metabolic regulators and components were more prominent in white or red muscle. Rats were treated with AICAR (1 mg/g body weight/day) for 14 days, resulting in increased expression levels of nicotinamide phosphoribosyltransferase (NAMPT), peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), glucose transporter 4 proteins, and enhanced mitochondrial biogenesis. These changes were more prominent in white rather than red gastrocnemius muscle or were only observed in the white gastrocnemius. Our results suggest that AICAR induces the expression of metabolic regulators and components, especially in type II (B) fibers.

Original languageEnglish
Pages (from-to)121-130
Number of pages10
JournalJournal of Physiological Sciences
Volume65
Issue number1
DOIs
Publication statusPublished - Jan 1 2015

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Aminoimidazole Carboxamide
Muscles
Organelle Biogenesis
Skeletal Muscle
Nicotinamide Phosphoribosyltransferase
Peroxisome Proliferator-Activated Receptors
AMP-Activated Protein Kinases
Facilitative Glucose Transport Proteins
Muscle Cells
Fatty Acids
Body Weight
Glucose
4-aminoimidazole
Proteins

All Science Journal Classification (ASJC) codes

  • Physiology

Cite this

A comparison of chronic AICAR treatment-induced metabolic adaptations in red and white muscles of rats. / Suwa, Masataka; Nakano, Hiroshi; Radak, Zsolt; Kumagai, Shuzo.

In: Journal of Physiological Sciences, Vol. 65, No. 1, 01.01.2015, p. 121-130.

Research output: Contribution to journalArticle

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