Journal
JOURNAL OF INFLAMMATION-LONDON
Volume 16, Issue -, Pages -Publisher
BMC
DOI: 10.1186/s12950-019-0221-3
Keywords
Obesity; Inflammation; Muscle; Atrophy; Fibroblast growth factor 21
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Funding
- Korea Food Research Institute [KFRI E0160500-02]
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Education [2018R1D1A1B07041643]
- Priority Research Centers Program of the NRF - Ministry of Education, Science and Technology [2014R1A6A1030318]
- National Research Foundation of Korea [2018R1D1A1B07041643] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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BackgroundObesity-induced skeletal muscle inflammation is a major contributor of skeletal muscle loss/atrophy and is implicated in metabolic complications such as insulin resistance. Fibroblast growth factor 21 (FGF21) is known to be an important metabolic regulator with anti-inflammatory properties. However, the effect of FGF21 on skeletal muscle atrophy is unclear. In this study, we investigated the effect of FGF21 deficiency on obesity-induced skeletal muscle inflammation and atrophy in mice.ResultsThe expression of atrophic factors (MuRF1 and Atrogin-1) was upregulated at the mRNA and/or protein levels in the skeletal muscle of FGF21-deficient obese mice compared with wild type obese control mice. This was accompanied by an increase in levels of inflammatory cytokines (TNF alpha and MCP-1) and a reduction in AMPK phosphorylation. FGF21 treatment markedly suppressed TNF alpha-mediated inflammatory and atrophic responses in cultured myotubes, and the actions of FGF21 were blunted by the AMPK inhibitor compound C.ConclusionThese findings suggest that FGF21 deficiency aggravates obesity-induced inflammation and atrophic responses in the skeletal muscle of obese mice, and FGF21 may protect inflammation-mediated atrophy through the AMPK pathway.
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