Carvacrol prevents diet-induced obesity by modulating gene expressions involved in adipogenesis and inflammation in mice fed with high-fat diet.

Carvacrol (2-methyl-5-isopropylphenol) is a monoterpene phenolic constituent of the essential oil produced by numerous aromatic plants and spices. The main objective of this study was to investigate effects of carvacrol in mice fed with a high-fat diet (HFD), which is an important model of obesity, and to study the potential underlying mechanisms focusing on the gene expression involved in adipogenesis, thermogenesis and inflammation. Male C57BL/6N mice were divided in three groups: those who received a normal diet, those fed with HFD and those fed with 0.1% carvacrol-supplemented diet (CSD). Body weight, visceral fat-pads and biochemical parameters were determined. Adipose tissue genes and protein expression levels were also assessed through reverse transcription polymerase chain reaction and Western blot analyses. Mice fed with CSD exhibited significantly reduced body weight gain, visceral fat-pad weights and plasma lipid levels compared with mice fed with HFD. Furthermore, HFD-induced up-regulations of adipose tissue genes and protein associated with the signaling cascades that lead to adipogenesis and inflammation were significantly reversed by dietary carvacrol supplementation. In summary, the major novel finding in our experimental conditions is that carvacrol prevented obesity in HFD-fed mice by decreasing body weight, visceral fat-pad weights and lowering plasma lipid levels. The evidence obtained in this study suggests that carvacrol appears to inhibit visceral adipogenesis probably by suppressing bone morphogenic protein-, fibroblast growth factor 1- and galanin-mediated signaling, and it also attenuates the production of pro-inflammatory cytokines in visceral adipose tissues by inhibiting toll like receptor 2 (TLR2)- and TLR4-mediated signaling.