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Life sciences · Journal article
Frontiers in Nutrition · October 22, 2026
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This study investigated the therapeutic effects of camel milk (CM) on high-fat diet (HFD)-induced obesity and its underlying mechanisms through integrative multi-omics analysis. C57BL/6J mice were fed a normal diet (NC), an HFD, or an HFD supplemented with CM via intragastric administration for 7 weeks, with orlistat as a positive control. CM treatment significantly reduced body weight, inguinal and epididymal white adipose tissue weights, serum triglyceride and LDL-C levels, and adipocyte hypertrophy compared to the HFD group. Additionally, CM ameliorated HFD-induced hepatic injury, as evidenced by reduced serum ALT levels and attenuated hepatic steatosis. 16S rRNA gene sequencing revealed that CM partially reversed HFD-induced gut microbiota dysbiosis, characterized by increased Bacteroidota abundance, suppression of pro-inflammatory genera ( Mucispirillum, Escherichia-Shigella, Faecalitalea ), and enrichment of the putative beneficial taxon unclassified [Eubacterium]_coprostanoligenes_group. Targeted metabolomics revealed that CM restored HFD-suppressed levels of colonic short-chain fatty acids (SCFAs), including acetic, butyric, and propionic acids. Untargeted liver metabolomics revealed that CM remodeled the hepatic metabolome, reversing HFD-induced elevations in sphingolipids [sphingosine, SM(d18:0/16:1(9Z))], and modulating lipid, glutathione metabolisms, and oxidative stress pathway. Liver transcriptomic analysis indicated that CM partially reversed HFD-induced gene expression changes, particularly downregulating genes involved in arachidonic acid metabolism (Cyp4a family), fatty acid elongation (Acot family), and glycerolipid metabolism ( Aldh3a2, Mgll, Mogat1 ), while modulating bile secretion genes. Spearman correlation analyses further revealed significant associations between CM-modulated gut microbial genera (notably unclassified [Eubacterium]_coprostanoligenes_group, Faecalitalea, and Escherichia-Shigella ) and obesity-related parameters, SCFA levels, hepatic metabolites, and lipid metabolism-related gene expression. These findings suggest that CM attenuates HFD-induced obesity and associated metabolic disturbances in association with gut microbiota modulation, enhanced SCFA production, and remodeling of hepatic lipid metabolism involving the gut-liver axis, pointing to CM as a potential dietary intervention for obesity management.