Intestinal metabolism of sulfur amino acids

Abstract

The gastrointestinal tract (GIT) is a metabolically significant site of sulfur amino acid (SAA) metabolism in the body and metabolises about 20 % of the dietary methionine intake which is mainly transmethylated to homocysteine and trans-sulfurated to cysteine. The GIT accounts for about 25 % of the whole-body transmethylation and trans-sulfuration. In addition, in vivo studies in young pigs indicate that the GIT is a site of net homocysteine release and thus may contribute to the homocysteinaemia. The gut also utilises 25 % of the dietary cysteine intake and the cysteine uptake by the gut represents about 65 % of the splanchnic first-pass uptake. Moreover, we recently showed that SAA deficiency significantly suppresses intestinal mucosal growth and reduces intestinal epithelial cell proliferation, and increases intestinal oxidant stress in piglets. These recent findings indicate that intestinal metabolism of dietary methionine and cysteine is nutritionally important for intestinal mucosal growth. Besides their role in protein synthesis, methionine and cysteine are precursors of important molecules. S-adenosylmethionine, a metabolite of methionine, is the principal biological methyl donor in mammalian cells and a precursor for polyamine synthesis. Cysteine is the rate-limiting amino acid for glutathione synthesis, the major cellular antioxidant in mammals. Further studies are warranted to establish how SAA metabolism regulates gut growth and intestinal function, and contributes to the development of gastrointestinal diseases. The present review discusses the evidence of SAA metabolism in the GIT and its functional and nutritional importance in gut function and diseases.

Effect of short-term administration of methionine on the ovary and uterus in a rat

“…However, it seems that methionine itself does not have toxicity directly because no side effects are seen in patients with very high levels of methionine in their plasma (Riedijk et al 2007;Burrin and Stoll 2007;Bauchart-Thevret et al 2009). Thus, it seems that metabolites of methionine might be responsible for its toxicity (Sakino et al 2006).…”

Dietary cysteine is used more efficiently by children with severe acute malnutrition with edema compared with those without edema

“…In addition, because gut mucosal proteins and mucins are rich in cysteine (6), and they turnover at extremely fast rates,~100-140% per day (7,8), cysteine deficiency may be contributing significantly to the intestinal mucosal atrophy and reduced secretory mucins, and therefore to the impaired gut function and leakiness, observed in children with SAM (9). These structural and functional abnormalities will be more pronounced in those with edematous SAM on the basis of the evidence of more severe gut mucosal atrophy observed in this group than in children with nonedematous SAM (10).…”

Splanchnic tissues respond differently when piglets are offered a diet 30 % deficient in total sulfur amino acid for 10 days

“…Glutathione is an important antioxidant preventing cellular damage caused by reactive oxygen species such as free radicals and peroxides. It is mainly produced in the intestine, liver, pancreas, kidneys, and adrenals, after which it can be redistributed to other tissues [39,40]. Our results show that a deficient TSAA supply decreased the total glutathione concentration in the liver and proximal jejunum, whereas distal jejunum, ileum and kidneys were less affected.…”