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.