Consequences of intestinal resection.
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Biomedical subjects
Publications and source records attributed to F Kern.
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Weanling rats were fed diets which contained either no protein or 27% protein. In one experiment after 23-35 days both groups were given l-leucine-4,5-(3)H either intragastrically or intraperitoneally and then sacrificed 24 hr later. In a second experiment animals were given these diets for 21 days and sacrificed 3, 6, or 12 hr after either intragastric or intraperitoneal administration of the labeled leucine. In both experiments the intestinal mucosa of proximal and distal segments of the small intestine was scraped, weighed, the protein concentration measured, and the specific activty of the mucosal protein was determined. The wet weight of the mucosa and the protein concentration of the mucosa were significantly greater in the control animals than in the protein-depleted animals. The mucosal protein per 100 g of body weight was the same in the protein-deprived and the control groups. The specific activity of the intestinal mucosal protein was higer in the protein-deprived animals than in the control animals. In the protein-deprived animals the proximal segment incorporated more radioactive amino acid into mucosal protein than did the distal segment at 3, 6, 12, and 24 hr after the amino acid was given by mouth. A similar difference was found between the proximal and distal segments of the control animals 6 hr after oral adminisstration of l-leucine-(3)H. On the other hand, when the l-leucine-(3)H was given intraperitoneally to both groups of animals there was no difference between proximal and distal small intestine. These findings suggest that intestinal mucosal protein can be synthesized directly from intraluminal amino acids, especially during protein deprivation, and that endogenous intraluminal protein might be important in the nutrition of the small intestinal mucosa.
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Fecal bile salt excretion was studied in healthy volunteers, patients with regional ileitis, and patients with ileal resection. 10 muc of carboxyl-(14)C-cholic acid was given orally. Stools and urine were collected daily for 5-10 days, the bile salts extracted, and the radioactivity assayed. Urinary excretion was negligible. All patients with ileal resection excreted bile salts in the feces significantly faster than controls, and five of the six excreted 50% of the radioactivity within 24 hr. Their mean intestinal transit time was 5.6 hr compared to 26 hr for the controls. Two of the three patients with regional ileitis excreted bile salts almost as rapidly as patients with ileal resection. Vitamin B(12) absorption was also defective in those patients, but the intestinal transit time was not decreased. To study the effect of rapid intestinal transit on bile salt excretion, four of the control subjects were given orally 1200 ml of 10% mannitol for 7 days, and the labeled cholic acid excretion rate was again studied. The mean intestinal transit time was markedly shortened, mild steatorrhea developed, and the fecal bile salt excretion rate increased slightly. It is concluded that ileal resection and ileal disease are major factors and rapid intestinal transit is a minor factor in causing excessive fecal bile salt loss. The relevance of bile salt wastage to lipid malabsorption is unknown because of insufficient information about compensatory jejunal absorption, maximum rate of hepatic bile salt synthesis, and the minimum necessary intraluminal concentration of conjugated bile salt.
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