Work

Mesona chinensis Benth polysaccharides alleviate type 2 diabetes mellitus in mice through gut microbiota and metabolic modulation

Year: 2026

Type: article

Abstract: Natural polysaccharides show considerable promise in the management of type 2 diabetes mellitus (T2DM). Mesona chinensis Benth polysaccharides (MP), traditionally consumed in East Asia for their metabolic benefits, exhibit anti-diabetic potential, although their mechanisms of action remain incompletely defined. This study investigated the therapeutic effects of MP and elucidated the underlying mechanisms, with a focus on the intestinal–metabolic axis in a T2DM mouse model. The chemical composition of MP was first characterized, followed by evaluation of its in vivo efficacy in modulating pancreatic β-cell function, systemic oxidative stress, inflammatory responses, and gut microbiota composition. MP was found to consist predominantly of galactose (31.3%) and galacturonic acid (32.6%). In T2DM mice, MP treatment effectively alleviated pancreatic β-cell damage, reduced oxidative stress, and suppressed inflammatory responses. Moreover, MP markedly reshaped the gut microbiota, notably increasing the abundance of Dorea and Bifidobacterium , and regulated associated lipid and energy metabolic pathways. Collectively, these results demonstrate that MP exerts pronounced anti-diabetic effects by restoring host metabolic homeostasis through coordinated modulation of the gut–metabolic axis. These findings support the potential application of MP as a functional food ingredient for the prevention and management of T2DM. • MP is rich in galactose (31.3%) and galacturonic acid (32.6%). • The anti-T2DM activity of MP was demonstrated through animal experiments. • MP modulated Dorea and Bifidobacterium at genus level. • MP upregulated fatty acids, SCFAs, and energy metabolism-related intermediates. • MP affected host metabolic function by enriching in glycine/serine/threonine metabolism and butanoate metabolism.

Source: Journal of Functional Foods

DOI: 10.1016/j.jff.2026.107216