Role of Coprophagy in Masking Dietary Deficiencies of Cystine in the Rat

Abstract

When a diet containing raw soybean was fed to rats, there was an increase in the synthesis of pancreatic protein, presumably exocrine protein, as evidenced by an increased uptake of [35S]cystine. There was also an increased transsulfuration of methionine sulfur as indicated by labeled sulfur transformation from methionine to cystine. This same pattern of events was produced in rats receiving a casein-containing diet when 50 mg of crystalline trypsin inhibitor was administered by gavage. However, if coprophagy was prevented, the increased uptake of [35S]cystine and [35S]methionine transsulfuration under both dietary conditions was blocked. It was found that prevention of coprophagy was without effect upon these two processes if supplementary dietary cystine was provided or if a dietary protein source with adequate cystine, i.e., heat-treated soybean, was provided. It was concluded that by practicing coprophagy, sufficient fecal cystine was being returned to the upper intestinal tract to permit some synthesis of pancreatic exocrine protein and with this stimulation of synthesis, transulfuration could proceed. This assumes that the biosynthesis of cystine is dependent upon the availability of sufficient cystine to permit active protein synthesis. In another situation where cystine requirement is high, namely, the rapidly growing rat, a limited amount of cystine was fed by providing a 12% casein diet. Either supplementary cystine or methionine was provided and it was found that both amino acids gave optimal growth in conventional rats, but when coprophagy was prevented, optimal growth was achieved only with the cystine-supplemented diet.