ArticleJCI insight2024
Downregulation of adipose LPL by PAR2 contributes to the development of hypertriglyceridemia.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Macrophage migration inhibitory factor as an indicator of chronic inflammation and metabolic risk in women.Biomedical reports · 2026Article
- Proteinase-Activated Receptor 2 (PAR2) Deficiency and Cardiovascular Regulation: Context-Dependent Effects on Inflammation and Fibrosis.Current issues in molecular biology · 2026Review
- Lipid Profile Alterations Across Coronary Heart Disease, Metabolic Syndrome, and Nephrotic Syndrome.Journal of clinical laboratory analysis · 2026Article
- REAC RGN-AR treatment modulates adipogenic differentiation in adipose tissue-derived stem cells.Scientific reports · 2026Article
- Comparison of the TyG index, TyG-traditional obesity indices, and TyG-novel obesity indices: does increased complexity help in predicting cardiometabolic multimorbidity?Lipids in health and disease · 2025Article
- The Role of Lysyl Oxidase in the Pathological Stage of Atherosclerosis: Structural Stabilizer or Disease Driver?Current atherosclerosis reports · 2025Review
- Poly-L-Lactic Acid Filler Increases Adipogenesis and Adiponectin in Aged Subcutaneous Tissue.Polymers · 2025Article
- Omega-3 fatty acid regulation of lipoprotein lipase and FAT/CD36 and its impact on white adipose tissue lipid uptake.Lipids in health and disease · 2024Review
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Authors and funding
16 authors.
Funding
Abstract
Lipoprotein lipase (LPL) hydrolyzes circulating triglycerides (TGs), releasing fatty acids (FA) and promoting lipid storage in white adipose tissue (WAT). However, the mechanisms regulating adipose LPL and its relationship with the development of hypertriglyceridemia are largely unknown. WAT from obese humans exhibited high PAR2 expression, which was inversely correlated with the LPL gene. Decreased LPL expression was also inversely correlated with elevated plasma TG levels, suggesting that adipose PAR2 might regulate hypertriglyceridemia by downregulating LPL. In mice, aging and high palmitic acid diet (PD) increased PAR2 expression in WAT, which was associated with a high level of macrophage migration inhibitory factor (MIF). MIF downregulated LPL expression and activity in adipocytes by binding with CXCR2/4 receptors and inhibiting Akt phosphorylation. In a MIF overexpression model, high-circulating MIF levels suppressed adipose LPL, and this suppression was associated with increased plasma TGs but not FA. Following PD feeding, adipose LPL expression and activity were significantly reduced, and this reduction was reversed in Par2-/- mice. Recombinant MIF infusion restored high plasma MIF levels in Par2-/- mice, and the levels decreased LPL and attenuated adipocyte lipid storage, leading to hypertriglyceridemia. These data collectively suggest that downregulation of adipose LPL by PAR2/MIF may contribute to the development of hypertriglyceridemia.
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