Abstract
Background: Accumulating evidence shows that high fat diet is closely associated with inflammatory bowel disease. However, the effects and underlying mechanisms of maternal high fat diet (MHFD) on the susceptibility of offspring to colitis in adulthood lacks confirmation.Methods: C57BL/6 pregnant mice were given either a high fat (60 E% fat, MHFD group) or control diet [10 E% fat, maternal control diet (MCD) group] during gestation and lactation. The intestinal development, mucosal barrier function, microbiota, and mucosal inflammation of 3-week old offspring were assessed. After weaning all mice were fed a control diet until 8 weeks of age when the microbiota was analyzed. Offspring were also treated with 2% DSS solution for 5 days and the severity of colitis was assessed.Results: The offspring in MHFD group were significantly heavier than those in MCD group only at 2–4 weeks of age, while no differences were found in the body weight between two groups at other measured time points. Compared with MCD group, MHFD significantly inhibited intestinal development and disrupted barrier function in 3-week old offspring. Although H&E staining showed no obvious microscopic inflammation in both groups of 3-week old offspring, increased production of inflammatory cytokines indicated low-grade inflammation was induced in MHFD group. Moreover, fecal analysis of the 3-week old offspring indicated that the microbiota compositions and diversity were significantly changed in MHFD group. Interestingly after 5 weeks consumption of control diet in both groups, the microbiota composition of offspring in MHFD group was still different from that in MCD group, although the bacterial diversity was partly recovered at 8 weeks of age. Finally, after DSS treatment in 8-week old offspring, MHFD significantly exacerbated the severity of colitis and increased the production of proinflammatory cytokine.Conclusions: Our data reveal that MHFD in early life can inhibit intestinal development, induce dysbiosis and low-grade inflammation and lead to the disruption of intestinal mucosal barrier in offspring, and enhance DSS-induced colitis in adulthood.
Highlights
The incidence and prevalence of IBD, a chronic immunologically mediated intestinal disorder including ulcerative colitis (UC) and Crohn’s disease (CD), has been increasing worldwide, especially in Asia [1,2,3]
maternal high fat diet (MHFD) significantly altered the composition of offspring intestinal microbiota and further enhanced the susceptibility to Dextran sulfate sodium (DSS)-induced colitis in adulthood. These findings suggest that MHFD in early life can negatively impact intestinal development and function, as well as cause a marked shift in gut microbiota, and predispose the offspring to facilitate the development of colitis
As villi length is commonly accepted for evaluation of intestinal growth [31], we examined morphological expressions to determine the intestinal growth of offspring in both groups
Summary
The incidence and prevalence of IBD, a chronic immunologically mediated intestinal disorder including ulcerative colitis (UC) and Crohn’s disease (CD), has been increasing worldwide, especially in Asia [1,2,3]. This epidemiological evolution has been paralleled with westernized diets and lifestyles [4]. Recent studies suggest that the intrauterine environment and placenta is not sterile as once presumed, the initiation period of neonate microbiome colonization remains obscure [11,12,13]. The effects and underlying mechanisms of maternal high fat diet (MHFD) on the susceptibility of offspring to colitis in adulthood lacks confirmation
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