PLIN2 inhibits insulin-induced glucose uptake in myoblasts through the activation of the NLRP3 inflammasome
Open accessAbstract
Impaired lipid metabolism and inflammatory pathways have individually been implicated in the development of insulin resistance in skeletal muscle; however, little evidence is available to date linking the two in this context. In this study, we explored a potential molecular mechanism underlying insulin resistance in myoblasts mediated by the crosstalk between lipid accumulation and inflammatory pathways. We examined the influence of perilipin 2 (PLIN2), one of the most highly expressed lipid droplet-associated proteins in skeletal muscle, on glucose uptake and on the nucleotide‑binding domain, leucine‑rich repeat containing protein 3 (NLRP3) inflammasome in vitro. PLIN2 overexpression in C2C12 cells led to an increased expression of NLRP3, caspase‑1 and interleukin (IL)‑1β, along with an impaired insulin‑induced glucose uptake. This defect was remedied by the RNAi‑mediated knockdown of NLRP3 expression. We also found that insulin receptor substrate‑1 (IRS‑1), a component of insulin signaling, was negatively regulated by NLRP3 and IL‑1β, and that IL‑1β inhibited insulin‑induced glucose uptake in myoblasts. These results suggest that PLIN2 inhibits insulin‑induced glucose uptake by activating NLRP3, caspase‑1 and IL‑1β, leading to a decreased IRS‑1 expression. This study provides in vitro evidence supporting an association between lipid metabolism and inflammatory pathways in the pathogenesis of insulin resistance in skeletal muscle, and suggests potential therapeutic targets that warrant further investigation.
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In cultured myocytes, a lipid droplet-associated protein perilipin 2 increases expression of NLRP3 inflammasome, resulting in impaired insulin-stimulated glucose uptake.
“In cultured myocytes, a lipid droplet-associated protein perilipin 2 increases expression of NLRP3 inflammasome, resulting in impaired insulin-stimulated glucose uptake [37].”
From Sarcopenic obesity, insulin resistance, and their implications in cardiovascular and metabolic consequences (2020) · cites this paper as [37]
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- Authors
- CHO, K.-A., & KANG, P. B.
- Affiliations
- University of Florida Health (US)
- ORCID
- KANG, PETER B.
- Venue
- International Journal of Molecular Medicine
- Publisher
- Spandidos Publications
- Published
- 2015-07-08
- Volume
- 36
- Issue
- 3
- Pages
- 839-844
- ISSN
- 1107-3756 (ISSN-L)
- 1791-244X
- OpenAlex
- W2133864400
- Cited by
- 43
- References
- 29
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 5 · 2023: 4 · 2022: 5 · 2021: 7 · 2020: 4 · 2019: 3 · 2018: 3 · 2017: 5 · 2016: 4
- FWCI
- 1.74
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- International Journal of Molecular Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Florida
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- PLIN2, NLRP3 inflammasome, insulin resistance, skeletal muscle, myoblasts, lipid droplets, lipid metabolism, inflammation, caspase-1, IL-1β, IRS-1, C2C12 myoblasts
- MeSH terms
- Perilipin-2, NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Biological Transport, Carrier Proteins, Cell Line, Glucose, Humans, Insulin, Insulin Resistance, Membrane Proteins, Transfection, Triglycerides, Up-Regulation, Myoblasts, Mice, Interleukin-1beta, Inflammasomes
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