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Increasing evidence shows that gut microbiota composition is related to changes of gut barrier function including gut permeability and immune function. Gut microbiota is different in obese compared to lean subjects, suggesting that gut microbes are also involved in energy metabolism and subsequent nutritional state. While research on gut microbiota and gut barrier has presently mostly focused on intestinal inflammatory bowel diseases and more recently on obesity and type 2 diabetes, this review aims at summarizing the present knowledge regarding the impact, in vivo, of depleted nutritional states on structure and function of the gut epithelium, the gut-associated lymphoid tissue (GALT), the gut microbiota and the enteric nervous system. It highlights the complex interactions between the components of gut barrier in depleted states due to food deprivation, food restriction and protein energy wasting and shows that these interactions are multidirectional, implying the existence of feedbacks.

Rationale: Nutritional disorders are often associated with a high risk to develop cardiovascular diseases, endothelial dysfunction being an early key marker. Changing the gut microbiota by prebiotics counteracts metabolic diseases. The work tests the hypothesis of a potential impact of prebiotics on the endothelial dysfunction induced by a nutritional depletion in n-3 polyunsaturated fatty acids (PUFA) in ApoE-/- mice. Methods: C57Bl/6J (WT) and ApoE-/- (KO) mice were fed a n-3 PUFA depleted-diet (DEF) for 12 weeks. For the last 15 days, WT and KO mice were or not supplemented with prebiotics (PRE). The vascular function was evaluated in mesenteric and carotid arteries. Circulating HbNO adducts were assessed by EPR. Results: The n-3 PUFA depletion induced an endothelial dysfunction in KO-DEF mesenteric arteries, as attested by a significant decrease of endothelial-dependent relaxation compared to WT DEF. Interestingly, PRE treatment in this group was able to improve the endothelial function by restoring the endothelial-dependent relaxation. PRE treatment in KO-DEF mice also lead to a vessel enlargement, to an increased intima-media thickness in the 2nd order mesenteric arteries, to an increased basal tone and a better KCl-induced contractibility of mesenteric arteries, compared to non-supplemented KO DEF mice. More, circulating HbNO was increased in KO-DEF-PRE mice and an improvement of endothelial function was also observed in carotid arteries. Conclusion: Our results demonstrated an outward remodeling and an improvement of the endothelial dysfunction in mesenteric arteries following prebiotic supplementation, probably due to activation of NO/NOS pathway. Data are in progress to evaluate how changes in the gut microbiota composition and function act on vascular function. This supports a novel therapeutic role for dietary prebiotics in the control of cardiovascular disease risk

effects of Elental® on the 5-FU treated HaCaT cells were examined by MTT assay and wound healing assay. Cellular migration ability was detected by using Boyden chamber. Moreover, the expression of FGF2 was examined by Western blotting. The production of FGF2 into the culture medium was quantified by ELISA. Results: Treatment with Elental® reduced oral mucositis and dermatitis more effectively than dextrin of the same caloric value in the animal model. MTT assay revealed the growthpromoting effect of Elental® on 5-FU treated HaCaT. In addition, Elental® could enhance the invasive capacity and migration ability of HaCaT as observed by wound healing assay and migration assay respectively. Moreover, ELISA and Western blotting showed up-regulated FGF2 in Elental® treated HaCaT. Conclusion: These findings suggest that Elental® is effective in the treatment of mucositis and dermatitis, and it may accelerate the mucosal and skin recovery through the induction of FGF2 and by reepithelization.