Abstract
Background: Concerns are emerging that a high-fat diet rich in n-6 PUFA (n-6HFD) may alter gut microbiome and increase the risk of intestinal disorders. Research is needed to model the relationships between consumption of an n-6HFD starting at weaning and development of gut dysbiosis and colonic inflammation in adulthood. We used a C57BL/6J mouse model to compare the effects of exposure to a typical American Western diet (WD) providing 58.4%, 27.8%, and 13.7% energy (%E) from carbohydrates, fat, and protein, respectively, with those of an isocaloric and isoproteic soybean oil-rich n-6HFD providing 50%E and 35.9%E from total fat and carbohydrates, respectively on gut inflammation and microbiome profile. Methods: At weaning, male offspring were assigned to either the WD or n-6HFD through 10–16 weeks of age. The WD included fat exclusively from palm oil whereas the n-6HFD contained fat exclusively from soybean oil. We recorded changes in body weight, cyclooxygenase-2 (COX-2) expression, colon histopathology, and gut microbiome profile. Results: Compared to the WD, the n-6HFD increased plasma levels of n-6 fatty acids; colonic expression of COX-2; and the number of colonic inflammatory and hyperplastic lesions. At 16 weeks of age, the n-6HFD caused a marked reduction in the gut presence of Firmicutes, Clostridia, and Lachnospiraceae, and induced growth of Bacteroidetes and Deferribacteraceae. At the species level, the n-6HFD sustains the gut growth of proinflammatory Mucispirillum schaedleri and Lactobacillus murinus. Conclusions: An n-6HFD consumed from weaning to adulthood induces a shift in gut bacterial profile associated with colonic inflammation.
Highlights
These concerns stem from evidence that adherence to other dietary patterns rich in monounsaturated fatty acids (MUFA) and n-3 PUFA [9] and lower in n-6 PUFA lower the risk of gut inflammation [10]
Most rodent studies modeling human consumption of n-6 high-fat diet (n-6HFD) have focused on short-term feeding (~2–8 weeks) [13,14,15,16,17,18], whereas rodent gut investigations of microbial ecology modeling human consumption of n-6HFD by young adult (8–12 weeks) to adult (>12 weeks) [19] are scarce. To address this knowledge gap, the objective of this study was to examine, in a mouse model, the effects of feeding an n-6HFD, from weaning to adulthood, on endpoints of colonic inflammation and gut microbiome profile compared to those elicited by a Western diet (WD)
By 16 weeks of age, animals on the n-6HFD diet gained on average ~25% more weight than those on the WD (Figure 1), with body weight gains between the two groups diverging significantly, starting at 10 weeks and increasing thereafter
Summary
Concerns have emerged that a high-fat diet (HFD) rich in n-6 PUFA (n-6HFD) exacerbate the risk of intestinal diseases [6,7] and obesity [8]. These concerns stem from evidence that adherence to other dietary patterns rich in monounsaturated fatty acids (MUFA) and n-3 PUFA [9] and lower in n-6 PUFA lower the risk of gut inflammation [10]. Concerns are emerging that a high-fat diet rich in n-6 PUFA (n-6HFD) may alter gut microbiome and increase the risk of intestinal disorders. The n-6HFD sustains the gut growth of proinflammatory Mucispirillum schaedleri and Lactobacillus murinus
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