METRNL attenuates lipid-induced inflammation and insulin resistance via AMPK or PPARδ-dependent pathways in skeletal muscle of mice
Open accessAbstract
Physical activity has many beneficial effects on metabolic disorders, such as obesity, insulin resistance, and diabetes. Meteorin-like protein (METRNL), a novel secreted protein homologous to the neurotrophin Metrn, is induced after exercise in the skeletal muscle. Herein, we investigated the effects of METRNL on lipid-mediated inflammation and insulin resistance in skeletal muscle via AMP-activated protein kinase (AMPK) or peroxisome proliferator-activated receptor δ (PPARδ). Treatment with METRNL suppressed inflammatory markers, such as nuclear factor κB (NFκB) nuclear translocation, inhibitory κBα (IκBα) phosphorylation, interleukin-6 (IL-6) expression, and pro-inflammatory cytokines (such as TNFα and MCP-1). METRNL treatment also attenuated the impaired insulin response both in palmitate-treated differentiated C2C12 cells and the skeletal muscle of high-fat diet (HFD)-fed mice. Furthermore, METRNL administration rescued glucose intolerance and reduced HFD-induced body weight gain in mice; however, METRNL did not affect calorie intake. METRNL treatment increased AMPK phosphorylation and PPARδ expression both in differentiated C2C12 cells and mouse skeletal muscle. siRNA-mediated suppression of AMPK and PPARδ abrogated the suppressive effects of METRNL on palmitate-induced inflammation and insulin resistance. Moreover, METRNL augmented the mRNA expression of fatty acid oxidation-associated genes, such as carnitine palmitoyltransferase 1 (CPT1), acyl-CoA oxidase (ACO), and fatty acid binding protein 3 (FABP3). siRNAs for AMPK and PPARδ reversed these changes. In the current study, we report for the first time that METRNL alleviates inflammation and insulin resistance and induces fatty acid oxidation through AMPK or PPARδ-dependent signaling in skeletal muscle.
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The myokines METRNL and BAIBA have proven to suppress TNF-α and other proinflammatory cytokines both in vitro and in vivo.
“Similarly, the myokines METRNL [100] and BAIBA [110] have proven to suppress TNF-α and other proinflammatory cytokines both in vitro and in vivo (5).”
From The Role of Exercise in the Interplay between Myokines, Hepatokines, Osteokines, Adipokines, and Modulation of Inflammation for Energy Substrate Redistribution and Fat Mass Loss: A Review (2020) · cites this paper as [100]
The Results section reports that METRNL reduced IL-6 expression in cultured C2C12 cells and serum TNFα and MCP-1 in high-fat-diet-fed mice. This supports the METRNL portion of the sentence across in vitro and in vivo settings, but the paper does not show TNFα suppression in vitro. BAIBA has a separate citation and is not assessed here. (LLM, conf=0.84)
Experimental — accuracy not yet measuredMETRNL enhances oxidative metabolism in skeletal muscle and white adipose tissue browning.
“enhance oxidative metabolism in SkM and WAT “browning” [100]”
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- Authors
- Jung, T. W., Lee, S. H., Kim, H.-C., Bang, J. S., Abd El-Aty, A. M., Hacımüftüoğlu, A., Shin, Y. K., & Jeong, J. H.
- Affiliations
- Seoul National University Bundang Hospital (KR)
- Chung-Ang University (KR)
- Kangwon National University (KR)
- Sookmyung Women's University (KR)
- Atatürk University (TR)
- Corresponding author
- Shin, Yong Kyoo
- Jeong, Ji Hoon
- ORCID
- Venue
- Experimental & Molecular Medicine
- Published
- 2018-09
- Volume
- 50
- Issue
- 9
- Pages
- 1-11
- ISSN
- 1226-3613 (ISSN-L)
- 2092-6413
- PMC
- PMC6137187
- OpenAlex
- W2890380917
- Cited by
- 203
- References
- 49
- Citations by year
- 2026: 25 · 2025: 47 · 2024: 29 · 2023: 37 · 2022: 19 · 2021: 19 · 2020: 15 · 2019: 12
- FWCI
- 4.09
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Experimental & Molecular Medicine (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Greater South Information System
- Funders
- National Research Foundation of Korea (2016R1C1B2012674)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- Metrnl, meteorin-like protein, skeletal muscle, insulin resistance, AMPK, PPARδ, fatty acid oxidation, high-fat diet, impaired glucose tolerance, NF-κB signaling, interleukin-6, obesity
- MeSH terms
- Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Animals, Cell Differentiation, Cell Line, Hyperlipidemias, Inflammation, Insulin Resistance, Lipids, Male, Mice, Inbred C57BL, Nerve Growth Factors, Signal Transduction, Muscle, Skeletal, Palmitic Acid, Muscle Cells, PPAR delta, AMP-Activated Protein Kinases, Diet, High-Fat, Endoplasmic Reticulum Stress
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