Lactiplantibacillus plantarum IMC 510 supplementation promotes colonic well-being in animal models of cafeteria-induced obesity.

Obesity is a persistent pathological condition characterized by excessive accumulation of adipose tissue, associated with a high risk of several morbidities and increased mortality. The link between excess calories and gut microbiota imbalance is well established, and alterations in this balance contribute to the promotion of chronic low-grade in-ammation. Our research aimed to examine the impact of a 12-week supplementation of Lactiplantibacillus (L.) plantarum IMC 510 (Lp) in rats fed a cafeteria diet (CAF), compared to those fed a standard diet (CHOW). To explore this aspect, the alterations in the gut microbiota were characterized, and the e.ects linked to the state of the colonic mucosa and enteric neuroplasticity were pointed out. Previously pub-lished data have shown that in the CAF Lp group, the probiotic maintained the predominant bacterial phyla in the composition of the intestinal microbiota compared to the CAF-fed rats [1]. Furthermore, Lp effectively reduced food intake and weight gain, with subsequent bene!cial e.ects highlighted by serological, biochemi-cal, and histological analyses. The CAF Lp group shows a signi!cant reduction in blood glucose and blood lipid profile, particularly lowering LDL [1]. Using various morphological staining techniques across the different experimental groups, no alterations in the architec-ture and structure of the colonic crypts were observed. In the CAF Lp group compared to the CAF-fed rats, a marked reduction in mucus secretion and composition, especially in the acid pro!le, was noted through stain-ing with Alcian Blue pH 2.5. A signi!cant reduction of Mucin-2, the major protein of the polymer network composed of gel-forming mucins, was associated with the administration of Lp. Concerning the enteric nervous system, no morpho-structural alterations of the myenter-ic plexuses were observed with the administration of Lp. A pan-neuronal marker was tested, revealing a decrease in immunoreaction that could be related to an alteration of intestinal motility [2]. By analyzing samples incubated with glial markers, the results indicate glial rearrangement in obesityrelated inammatory conditions. No rec-ognizable di.erences were found between experimental groups when discriminating cholinergic neurons within the myenteric plexus. In contrast, the nitrergic neuronal network underwent neurodegeneration in obese groups, possibly related, in accordance with other studies, to oxi-dative stress and in-ammatory status. In conclusion, the Lp intervention could represent a new strategy to counteract the negative e.ects induced by obesity-related dysbiosis, making this approach both novel and safe for the prevention and management of obesity.