Allicin attenuates diet-induced obesity in association with gut microbiota remodeling, fecal butyrate, and hepatic PPAR signaling in rats.

Abstract

Obesity is associated with gut microbial dysbiosis and impaired intestinal barrier function. Allicin, a garlic-derived organosulfur compound, has shown anti-obesity effects, but the links between its effects on gut microbial metabolism and hepatic gene expression remain unclear. This study examined the metabolic effects of allicin and associated gut-liver responses using microbiota profiling, targeted short-chain fatty acid (SCFA) metabolomics, hepatic transcriptomics, network pharmacology and quantitative PCR. Male Sprague-Dawley rats received oral allicin at 60 or 80 mg kg-1 day-1 for 4 weeks after 8 weeks of high-fat diet (HFD) feeding. Compared with HFD controls, both doses reduced body weight gain, improved glucose tolerance and serum lipid profiles, and lowered serum markers of hepatic injury. Allicin treatment also remodeled the gut microbiota by enriching Ligilactobacillus and Akkermansia and reducing Escherichia-Shigella, and increased fecal butyrate concentrations. These changes were accompanied by increased colonic expression of barrier-related and SCFA receptor genes and lower serum lipopolysaccharide concentrations. Hepatic transcriptomics and network pharmacology both implicated peroxisome proliferator-activated receptor (PPAR) signaling, with qPCR supporting expression changes in selected genes. Correlation analyses identified positive associations of fecal butyrate concentrations with the relative abundances of Ligilactobacillus and Akkermansia and with colonic barrier-related gene expression. Together, these findings support a proposed microbiota-butyrate-hepatic PPAR framework for further investigation of allicin as a potential functional food ingredient, while causal links among these components remain to be established.

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