The present study was designed to investigate the effect of embelin in metabolic endotoxemia (ME) mediated inflammation and associated obesity in high fat diet (HFD)-fed C57BL/6 mice. The molecular docking of embelin confirms its binding with the toll-like receptor-4 (TLR-4). In vivo study, mice were treated with HFD for 8 weeks to induce ME mediated inflammation and associated obesity. Further, mice were treated with embelin (50 and 100 mg/kg/day, p.o.) and orlistat (10 mg/kg/day, p.o.) from 5th to 8th week along with HFD to improve associated changes. After 8 weeks, mice were euthanized and assessed for body weight, body mass index (BMI), fat pad weights (mesenteric, retroperitoneal, and epididymal), intestinal permeability, TLR-4, tumor necrosis factor-α, interleukin-6, lipopolysaccharide, and serum lipid levels followed by histopathological analysis of liver and adipose tissues. Embelin significantly decreased the body weight, BMI, serum lipid levels, ME, and inflammation manifested by above parameters. Further, results of histopathological study showed that embelin restored the vacuolization, inflammation, one side shifting of nucleus in liver tissue, and decreased adipocyte cells size in adipose tissue in HFD-fed mice. Thus, our findings provide the strong evidence first time that embelin could modulate ME, mediate inflammation, and consequently reduce body weight gain, BMI, and serum lipid levels in HFD-fed mice.
Fructo-oligosaccharides lower serum lipid levels and suppress high-fat/high-sugar diet-induced inflammation by elevating serum and gut levels of short-chain fatty acids
