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Microbiota-accessible carbohydrates (MACs) exert health-promoting effects, but how each MAC impacts gut microbiota and regulates host physiology remains unclear. Here, we show that l -arabinose and sucrose cooperatively act on gut microbiota and exert anti-obesogenic effects. Specifically, l -arabinose, a monosaccharide that is poorly absorbed in the gut and inhibits intestinal sucrase, suppresses diet-induced obesity in mice in the presence of sucrose. Additionally, the suppressive effect of l -arabinose on adiposity is abrogated in mice lacking the short-chain fatty acid (SCFA) receptors GPR43 and GPR41. Mechanistically, l -arabinose increases the relative abundance of acetate and propionate producers (e.g., Bacteroides), while sucrose enhances SCFA production. Furthermore, l -arabinose and sucrose activate the glycolytic and pentose phosphate pathways of Bacteroides , respectively, indicating that they synergistically promote acetate production through distinct pathways. These findings suggest that each MAC has a unique property and thus may serve as a precision gut-microbiota modulator to promote host homeostasis. [Display omitted] • l -Arabinose suppresses adiposity in animals fed a high-fat diet with sucrose • l -Arabinose increases the relative abundance of acetate and propionate producers • Sucrose enhances the production of acetate and propionate induced by l -arabinose • l -Arabinose/sucrose activate distinct metabolic pathways of acetate-producing bacteria Microbiota-accessible carbohydrates (MACs) impact host physiology. Tomioka et al. demonstrate that two different MACs, l -arabinose and sucrose, act in concert on the gut microbiota to regulate short-chain fatty acid production and host metabolic functions. Furthermore, the two MACs stimulate distinct intracellular metabolic pathways of gut microbiota related to acetate production. [ABSTRACT FROM AUTHOR]

Metabolic syndrome (MetS) is a multifactorial chronic metabolic disorder that affects approximately one billion people worldwide. Recent studies have evaluated whether targeting the gut microbiota can prevent MetS. This study aimed to assess the ability of dietary fiber to control MetS by modulating gut microbiota composition. Sodium alginate (SA) is a seaweed-derived dietary fiber that suppresses high-fat diet (HFD)-induced MetS via an effect on the gut microbiota. We observed that SA supplementation significantly decreased body weight gain, cholesterol levels, and fat weight, while improving glucose tolerance in HFD-fed mice. SA changed the gut microbiota composition and significantly increased the abundance of Bacteroides. Antibiotic treatment completely abolished the suppressive effects of SA on MetS. Mechanistically, SA decreased the number of colonic inflammatory monocytes, which promote MetS development, in a gut microbiota-dependent manner. The abundance of Bacteroides was negatively correlated with that of inflammatory monocytes and positively correlated with the levels of several gut metabolites. The present study revealed a novel food function of SA in preventing HFD-induced MetS through its action on gut microbiota. [ABSTRACT FROM AUTHOR]