Key result
TLR2 knockout decreases adipose collagen I and related inflammatory factors versus wild-type obese mice.
TLR2 knockout reduces collagen I deposition and alters related metabolic markers in the adipose tissue of high-fat diet-induced obese mice.
TLR2 may be a target in obesity-related adipose fibrosis; these animal data leave open human translation.
Obesity is marked by deposition of collagen I in adipose tissue. Toll like receptor (TLR)2 is involved in lipid metabolism, however the association between TLR2 and collagen I remains unclear. The present study was designed to investigate the effect of TLR2 knockout on collagen I in adipose tissue in obese mice. TLR2 knockout and C57BL/6J mice (aged 4 weeks) were fed normal chow or a high‑fat‑diet for 16 weeks. Compared with adipose tissue from lean controls, that from C57BL/6J mice fed a high‑fat diet had increased levels of collagen I, TIMP1 and TGFβ1 and lower levels of MMP1. However, adipose tissue from TLR2 knockout mice fed a high‑fat diet revealed decreased levels of collagen I, TIMP metallopeptidase inhibitor (TIMP)1, and transforming growth factor (TGF)β1, in addition to increased levels of matrix metallopeptidase (MMP)1. These findings suggest that, in the adipose tissue of obese mice, TLR2 is involved in the metabolism of collagen I and may exhibit a role in the metabolism of MMP1, TIMP1 and TGFβ1.
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Song et al. (2018) studied Obesity. TLR2 knockout vs. Wild-type C57BL/6J mice was evaluated on Collagen I deposition and expression of related inflammatory and metabolic factors in adipose tissue. TLR2 knockout in mice fed a high-fat diet decreased levels of collagen I, TIMP1, and TGF-β1, and increased levels of MMP1 in adipose tissue compared to wild-type obese mice.
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