Changes in the small intestine ofSchistosoma mansoni-infected mice fed a high-fat diet

Abstract

The consumption of a high-fat diet modifies both the morphology of the small intestine and experimentally tested effects of schistosomiasis mansoni. However, whether a schistosomiasis infection associated with a high-fat diet causes injury to the small intestine has never been investigated. Mice were fed either a high-fat or a standard-fat diet for 6 months and were then infected with Schistosoma mansoni cercariae. Physical characteristics of the intestinal tissue (mucosal thickness, small intestinal villi length and height, and abundance of goblet cells and enterocytes on the villous surface) and the distribution of granulomas along the intestinal segments and their developmental stage were measured at the time of sacrifice (9 or 17 weeks post-infection). The group fed a high-fat diet exhibited different granuloma stages, whereas the control group possessed only exudative granulomas. The chronically infected mice fed a high-fat diet exhibited higher granuloma and egg numbers than the acutely infected group. Exudative, exudative/exudative-productive and exudative-productive granulomas were present irrespective of diet. Computer-aided morphometric analysis confirmed that villus length, villus width, muscular height and submucosal height of the duodenal and jejunal segments were affected by diet and infection. In conclusion, a high-fat diet and infection had a significant impact on the small intestine morphology and morphometry among the animals tested.

Glucagon-like peptide-2 and mouse intestinal adaptation to a high-fat diet

“…In our experimental model, mice chronically fed a HFD showed changes in some morphometric parameters, consistent with the results of the previous studies (Sagher et al 1991, Thomson et al 1996, Scoaris et al 2010, De Barros Alencar et al 2012, which were similar in duodenal and jejunal segments. Indeed, we cannot establish whether the effects observed are specifically induced by the fat or by the different caloric intake.…”

The modulatory role of high fat feeding on gastrointestinal signals in obesity

“…As such, there is a minimal change in the gene expression when the diet contains up to 20% energy from fat; however, the up-regulation of lipid metabolism-related genes increases accordingly with the percentage of fat in the diet [95]. HF feeding also leads to GI tract morphological changes including an increase in villi height and crypt depth and thicker microvilli, resulting in increased enterocytes per villus and enhanced capacity for fat absorption in the small intestine [96][97][98][99]. In line with increased hyperplasia and hypertrophy, one study demonstrated an increase in GIP-and GLP-1-expressing cells in the duodenum of HF fed rats [100]; however, other studies have found no difference [101,102].…”

Superimposing a high-fat diet on Schistosoma mansoni infection affects renin-angiotensin system components in the mouse kidney

“…The IHFD group that exhibited increased body weight after one week on the high-fat diet until two weeks before euthanasia showed an abrupt loss of body weight, likely because a high-fat diet in the acute phase of schistosomiasis, as in the present study, results in reduced villus length in the duodenum and an increased number of granulomas along the duodenum and jejunum 9 , affecting mouse nutrition. In S. mansoni, oviposition begins at 42 d post-infection when the worms become adults 24 .…”

“…The nutritional status of the host influences the S. mansoni cycle. For example, a host maintained on a low-protein diet elicits reproductive gland impairment and morphological changes in the worms 6,7 , while a host maintained on a high-fat diet is beneficial for the life cycle of the parasite 8,9 .…”