Muscle‐specific Perilipin2 down‐regulation affects lipid metabolism and induces myofiber hypertrophy
Open accessAbstract
Background: Perilipin2 (Plin2) belongs to a family of five highly conserved proteins, known for their role in lipid storage. Recent data indicate that Plin2 has an important function in cell metabolism and is involved in several human pathologies, including liver steatosis and Type II diabetes. An association between Plin2 and lower muscle mass and strength has been found in elderly and inactive people, but its function in skeletal muscle is still unclear. Here, we addressed the role of Plin2 in adult muscle by gain and loss of function experiments. Methods: By mean of in vivo Plin2 down‐regulation (shPlin2) and overexpression (overPlin2) in murine tibialis anterior muscle, we analysed the effects of Plin2 genetic manipulations on myofiber size and lipid composition. An analysis of skeletal muscle lipid composition was also performed in vastus lateralis samples from young and old patients undergoing hip surgery. Results: We found that Plin2 down‐regulation was sufficient to induce a 30% increase of myofiber cross‐sectional area, independently of mTOR pathway. Alterations of lipid content and modulation of genes involved in lipid synthesis occurred in hypertrophic muscles. In particular, we showed a decrease of triglycerides, ceramides, and phosphatidylcoline:phosphatidylethanolamine ratio, a condition known to impact negatively on muscle function. Plin2 overexpression did not change fibre size; however, lipid composition was strongly affected in a way that is similar to that observed in human samples from old patients. Conclusions: Altogether these data indicate that Plin2 is a critical mediator for the control of muscle mass, likely, but maybe not exclusively, through its critical role in the regulation of intracellular lipid content and composition.
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Alteration in lipid composition due to downregulation of Perilipin2 is sufficient to induce hypertrophy and prevent muscle atrophy after denervation, and this hypertrophy seems largely mTOR-independent because rapamycin did not prevent muscle growth after Perilipin2 knockdown.
“For instance, alteration in lipid composition due to the downregulation of the lipid-associated protein Perilipin2 is sufficient to induce hypertrophy and prevent muscle atrophy after denervation38. Interestingly, this type of hypertrophy seems to be largely mTOR-independent because rapamycin treatment did not prevent muscle growth after Perilipin2 knockdown.”
From Mechanisms of muscle atrophy and hypertrophy: implications in health and disease (2021) · cites this paper as [38]
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- Authors
- Conte, M., Armani, A., Conte, G., Serra, A., Franceschi, C., Mele, M., Sandri, M., & Salvioli, S.
- Affiliations
- University of Bologna (IT)
- Veneto Institute of Molecular Medicine (IT)
- University of Pisa (IT)
- IRCCS Institute of Neurological Sciences of Bologna Bologna Italy
- University of Padua (IT)
- Corresponding author
- Conte, Maria
- ORCID
- Venue
- Journal of Cachexia, Sarcopenia and Muscle
- Publisher
- Wiley
- Published
- 2018-10-04
- Volume
- 10
- Issue
- 1
- Pages
- 95-110
- ISSN
- 2190-5991 (ISSN-L)
- 2190-6009
- PMC
- PMC6438344
- OpenAlex
- W2895679601
- Cited by
- 30
- References
- 63
- Citations by year
- 2026: 7 · 2025: 4 · 2024: 1 · 2023: 1 · 2022: 8 · 2021: 5 · 2020: 4
- FWCI
- 0.80
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Journal of Cachexia Sarcopenia and Muscle (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- CINECA IRIS Institutial research information system (University of Pisa) (submittedVersion, other-oa)
- Archivio istituzionale della ricerca (Alma Mater Studiorum Università di Bologna) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Padua Research Archive (University of Padova) (submittedVersion)
- Funders
- H2020 European Research Council (282310‐MyoPHAGY)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Keywords
- skeletal muscle, muscle fiber hypertrophy, lipid metabolism, triglycerides, ceramide, muscle mass, sarcopenia, aging, tibialis anterior, vastus lateralis, mTOR signaling, fat deposition
- MeSH terms
- Perilipin-2, Adult, Aged, 80 and over, Animals, Female, Humans, Hypertrophy, Male, Mice, Inbred C57BL, Down-Regulation, Muscle, Skeletal, Lipid Metabolism
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