Jejunal transport in experimental nephrotic syndrome.
In vivo jejunal transport of amino acids, monosaccharides, sodium, and electrolytes were studied in rats made nephrotic with puromycin aminonucleoside (PAN) and in pair-fed controls. Studies were performed 14 days after a single intravenous dose of PAN when rats were no longer edematous, but were still hypoproteinemic. There was decreased absorption of glucose, 3-0-methyl glucose, glycine, phenylalanine, histidine, water, and sodium in the nephrotic animals but transport of fructose, lysine and potassium was similar in the nephrotic and control animals. Enzyme kinetic studies for glucose transport showed a mixed type of inhibition affecting both Vm and Km. The jejunal mucosa of nephrotic and control rats had similar ATP content and enzyme activity for lactase, sucrase, maltase and (Na-K)-ATPase and the ratios of RNA to DNA were similar in the nephrotic and control rats. No abnormality of the jejunum was detected by light or electron microscopy. The data suggest that the impairment of absorption is a result of decreased activity of jejunal membrane carrier mechanisms. The altered transport may be secondary to effects related to the metabolic consequences of nephrotic syndrome and does not appear to be related to acute purine aminonucleoside toxicity, edema or malnutrition.
D019325:3-O-Methylglucose; D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D005632:Fructose / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D007583:Jejunum / Q000201:enzymology / Q000378:metabolism*; D008297:Male; D008757:Methylglucosides / Q000378:metabolism; D009404:Nephrotic Syndrome / Q000201:enzymology / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000378:metabolism; D014867:Water / Q000378:metabolism
D000596:Amino Acids; D008757:Methylglucosides; D014867:Water; D019325:3-O-Methylglucose; D005632:Fructose; D012964:Sodium; D005947:Glucose; D011188:Potassium