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Obesity is associated with intestine dysbiosis and is characterized by a low-grade inflammatory status, which affects vascular function. In the present study, we evaluated the effects of a probiotic with immunomodulatory properties, Lactobacillus coryniformis CECT5711, in obese mice fed on an HFD (high-fat diet). The probiotic treatment was given for 12 weeks, and it did not affect the weight evolution, although it reduced basal glycaemia and insulin resistance. L. coryniformis administration to HFD-induced obese mice induced marked changes in microbiota composition and reduced the metabolic endotoxaemia as it decreased the LPS (lipopolysaccharide) plasma level, which was associated with a significant improvement in gut barrier disruption. Furthermore, it lowered TNFá (tumour necrosis factor á) expression in liver, improving the inflammatory status, and thus the glucose metabolism. Additionally, the probiotic reversed the endothelial dysfunction observed in obese mice when endothelium- and NO (nitric oxide)-dependent vasodilatation induced by acetylcholine in aortic rings was studied. It also restored the increased vessel superoxide levels observed in obese mice, by reducing NADPH oxidase activity and increasing antioxidant enzymes. Moreover, chronic probiotic administration for 2 weeks also improved endothelial dysfunction and vascular oxidative stress induced by in vivo administration of LPS in control mice fed on a standard chow diet. The results of the present study demonstrate an endothelial-protective effect of L. coryniformis CECT5711 in obese mice by increasing NO bioavailability, suggesting the therapeutic potential of this gut microbiota manipulation to prevent vasculopathy in obesity. [ABSTRACT FROM AUTHOR]

OA (osteoarthritis) is a degenerative condition associated with obesity. A number of metabolic explanations have been proposed to explain the association between obesity and OA in nonweight- bearing joints; however, none of these hypotheses have been demonstrated empirically. In the present Hypothesis article, we recognize that obesity is associated with compromised gut mucosa, translocation of microbiota and raised serum LPS (lipopolysaccharide). The consequent activation of the innate immune response leads to increased serum titres of inflammatory mediators in obese patients, with both local and systemic markers of inflammation associated with onset and progression of OA. Furthermore, a number of workers have shown that articular cartilage repair is impaired by a range of inflammatory mediators, both in vitro and in vivo. We propose that metabolic endotoxaemia, caused by impaired gastric mucosa and low-grade chronic inflammation, may contribute to the onset and progression of OA in obese patients. This may account for the association between obesity and OA at non-weight-bearing joints which cannot be explained by biomechanical factors. [ABSTRACT FROM AUTHOR]