Arbutin Reshapes Intestinal Microbiota to Ameliorate Lipid Metabolic Dysfunction and Inflammation.
TL;DR
It is established that arbutin ameliorates obesity-related inflammation and metabolic disorders via gut microbiota-derived SCFA production.
Abstract
Gut microbial dysbiosis drives obesity-related metabolic disorders. This study investigated whether arbutin, a phenolic glycoside, alleviates obesity via gut microbiota modulation. In obese mice, arbutin reduced body weight, improved glucose and lipid profiles, suppressed adipogenic and inflammatory gene expression, and strengthened intestinal barrier integrity. 16S rRNA sequencing revealed elevated α-diversity and enrichment of beneficial genera including Muribaculaceae and Lactobacillus. Antibiotic depletion abolished arbutin's antiobesity effects, whereas fecal microbiota transplantation from arbutin-treated donors recapitulated metabolic improvements and increased fecal short-chain fatty acids, including acetate, propionate, butyrate, and valerate, in a microbiota-dependent manner. Correlation analysis linked SCFA elevation to Muribaculaceae, Bacteroides, Lachnospiraceae_UCG-001, and Prevotellaceae_NK3B31_group, and KEGG enrichment implicated carbohydrate and lipid metabolism as the primary pathways affected. Collectively, these findings establish that arbutin ameliorates obesity-related inflammation and metabolic disorders via gut microbiota-derived SCFA production.