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B L Shneider

Publications and source records attributed to B L Shneider.

39 records · Page 3Linked to original sources
PubMed1993

The effects of bile acid feeding on the development of ileal bile acid transport.

Sodium-dependent bile acid uptake is developmentally regulated in the rat ileum. Transport activity is abruptly expressed on postnatal d 17, although the mechanisms controlling this expression are poorly understood. Changes in bile salt metabolism and hepatic transport result in a marked increase in bile flow before postnatal d 17, and thus this study examined the effects of bile salt feeding on the development of ileal bile acid transport. Twelve-d-old rat pups were gavage-fed saline, taurocholate, or mannitol on a daily basis for 3 d. Sodium-dependent bile acid transport was studied by rapid filtration using ileal brush-border membrane vesicles prepared from the various experimental groups. Taurocholate feeding resulted in precocious development of sodium-dependent bile acid transport and induction of sucrase activity. Mannitol feeding, used as a control for the effects of diarrhea-induced stress, resulted in similar sucrase activity, yet sodium-dependent bile acid transport was induced to only half the level observed in taurocholate-fed animals (3.2 +/- 1.6 versus 6.9 +/- 2.0 pmol/mg protein/45 s, p < 0.001). Serum corticosterone levels were similar in the mannitol- and taurocholate-fed animals (3.8 +/- 1.3 versus 4.6 +/- 1.8 micrograms/dL). Both feedings lead to histologic maturation of the ileum, with a more pronounced effect in the taurocholate-fed pups. Bile salt feeding induces precocious expression of ileal bile acid transport, apparently by both diarrhea-induced stress and a bile salt-specific effect.

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PubMed1991

An ontogenically regulated 48-kDa protein is a component of the Na(+)-bile acid cotransporter of rat liver.

Recent evidence suggests that the Na(+)-coupled carrier mechanism for bile acids on the hepatocyte basolateral plasma membrane is a polypeptide in the molecular weight range of 48,000-50,000. In this study we used a strategy for the identification and isolation of this transport protein based on the observation that Na(+)-dependent transport activity is abruptly expressed in fetal rat liver just before birth [Suchy et al. Am. J. Physiol. 251 (Gastrointest. Liver Physiol. 14): G665-G673, 1986]. Analysis of basolateral plasma membranes by SDS-PAGE revealed that a protein of apparent molecular weight 48,000 was absent from fetal rat liver on day 19 of gestation, barely detectable on day 20, and thereafter increased progressively with postnatal development. Monospecific, polyclonal antibodies raised against the 48-kDa protein but not preimmune antibodies significantly inhibited the initial rate of Na(+)-dependent taurocholate uptake by isolated rat hepatocytes. In contrast, Na(+)-independent taurocholate transport and uptake of another anion, 35SO4(2-), were not affected by antibody treatment. When an extract containing the total complement of basolateral proteins was incorporated into asolectin liposomes, Na+ gradient-dependent uptake of taurocholate was observed, including a 2- to 2.5-fold accumulation of substrate above its equilibrium concentration (overshoot). However, if the membrane extract was first selectively depleted of the 48-kDa protein by immunoprecipitation with the anti-48-kDa antibody before reconstitution, Na(+)-dependent stimulation of taurocholate transport was completely abolished. These studies indicate that an ontogenically regulated 48-kDa protein is a component of the basolateral Na(+)-dependent transport system for bile acids.

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