ArticleMolecular biology reports2022
Mechanism of protection from insulin resistance by toll-like receptor 2 deficiency in high-fat diet fed mice: involvement in macrophage polarization.
Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 3 citations in OpenAlex.
- Venous thrombosis and obesity: from clinical needs to therapeutic challenges.Internal and emergency medicine · 2025Review
- miR-335-3p improves type II diabetes mellitus by IGF-1 regulating macrophage polarization.Open medicine (Warsaw, Poland) · 2024Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundToll-like receptor 2 (TLR2) deficiency can increase insulin sensitivity and improves glucose tolerance. However, it is not yet fully understood about its underlying mechanism. The regulation of M1/M2 macrophage polarization has been verified to involve in insulin resistance. Here, we evaluated whether the beneficial effect of TLR2 deficiency is mediated by TLR2-associated macrophage polarization in mice fed with high-fat diet (HFD). METHODS AND
resultsWild-type and TLR2 knockout (TLR2
conclusionsOur results reveal that TLR2 knockout-mediated macrophages M2 polarization is a crucial factor for preventing against diet-induced insulin resistance in mice. These findings deepen our knowledge about the mechanism underlying HFD-induced insulin resistance.
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