Effects of methionine, tryptophan, and niacin deficient diets on gene expression in intestinal cells in the DSS drinking IBD mouse model.
Inflammatory bowel disease (IBD) is one of the intractable diseases. Nutritional components associated with IBD have been identified, and it is known that excessive methionine intake exacerbates inflammation and that tryptophan metabolism is involved in inflammation. In this study, we examined how temporary methionine, tryptophan, and niacin deficiencies alter gene expression in the intestinal cells of a dextran sulfate sodium (DSS)-fed IBD mouse model. The results showed that feeding amino acid deficient diets increased the expression of serine proteases and fat metabolizing enzymes. Amino acid deficiency also activated one-carbon metabolism and the PPAR pathway. These results suggest that temporary amino acid deficiency may be useful to enhance the antioxidant activity of the host. Overall design: To examine the effects of amino acid deficiency, total RNA was extracted from mouse intestinal tracts for 9 conditions (R, 1K, 2K, 3K, RR, 1KR, 2KR, 3KR, C) and RNA- seq was performed. 1K, 2K, and 3K were fed amino acid-deficient diets until day 28 of rearing, and intestinal tracts were collected. The 1KR, 2KR, and 3KR were fed amino acid-deficient diet until day 28, and then fed normal diet until day 33, when their intestinal tracts were collected. R was fed normal diet until day 28 and their intestinal tract was collected. RR was fed normal diet until day 33 and the intestinal tract was collected. R, 1K, 2K, 3K, RR, 1KR, 2KR, and 3KR were free-drinking DSS from day 18 of rearing. C was control mice reared on normal feed, and their intestinal tract was collected on day 34. 1K and 1KR were fed methionine-deficient diet until day 28. 2K and 2KR were fed tryptophan- and niacin-deficient diet until day 28. 3K and 3KR were fed methionine-, tryptophan-, and niacin-deficient diet until day 28.