Effect of Na⊕ on Bile Acid Uptake by Isolated Rat Hepatocytes

Anwer, Muhammad; Hegner, D.

doi:10.1515/bchm.1978.359.1.181

Cited by 44 publications

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“…Uptake of taurocholate at concentrations from 5-200 pM was linear in excess of 90 sec, similar to data reported by other investigators using hepatocytes from adult rats (4,35). Extrapolation of the uptake versus time plot yielded a positive intercept suggesting rapid initial adsorption of taurocholate to the plasma membrane.…”

Section: Resultssupporting

confidence: 87%

“…However, the Cfold increase in Vmax may reflect an increase in the number of transport or binding sites. The rate constants derived in 56-day-old rats are similar to those reported by other authors for the mature rat, e.g., a Km of 20-40 pM and a Vmax of 1.8-3.8 nmoles/min/mg protein (4,31,35). Stacey and Klaassen (40) have observed a similar pattern of development for ouabain uptake in isolated rat hepatocytes; Vmax increased gradually with postnatal age whereas Km values remained constant.…”

Section: Discussionsupporting

confidence: 88%

“…Studies performed in the isolated perfused rat liver and in isolated hepatocytes indicate that bile acid uptake is an active, sodium-dependent process (4,33). The initial interaction between bile acids and the liver cell occurs at the sinusoidal face of the surface membrane where a putative bile acid receptor has been identified (1).…”

Section: Discussionmentioning

confidence: 99%

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Uptake of Taurocholate by Hepatocytes Isolated from Developing Rats

Suchy

Balistreri

1982

Pediatr Res

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Summaryon Purina rat chow and water ad libitum. Male rats were utilizedTo further define developmental changes in bile acid metabolism, we determined the kinetics of taurocholate uptake by hepatocytes isolated from Sprague-Dawley rats at 7, 14,21,28, and 56 days of age. There was a progressive increase in taurocholate uptake with age. The uptake process exhibited saturable kinetics in every age group with a maximum uptake velocity attained above a taurocholate concentration of 200 pM. There were no differences in Km values but Vmax increased progressively between 7 and 56 days of age. These data suggest that the deficit in hepatic excretory function observed in immature mammals of several species may, in part, be related to decreased transport of bile acids. SpeculationImpaired transport of bile acids by the liver may limit bile flow during development and lead to inefficient fat digestion, altered hepatic excretion of drugs, and an increased susceptibility to cholestasis. Comparable Km values for the uptake process indicate that hepatocyte affinity for taurocholate remains constant during development; whereas the rise in Vmax with postnatal age may reflect an increase in the number of binding sites. Specific changes in the liver cell plasma membrane are likely to be important determinants of the ontogeny of bile acid transport and bile flow.Bile acids are major synthetic and excretory products of the liver and are of primary importance in the generation of bile flow (1 1, 15, 20). There is increasing evidence in humans and in experimental animals that the enterohepatic circulation of bile acids is not fully developed at birth and that the perinatal liver is normally subject to a period of "physiological cholestasis" (13,14,41). In the normal human infant and in the suckling rat, bile acid pool size is decreased (42, 44) and the concentration of bile acids in serum is elevated (5, 6, 41). As a consequence of decreased bile secretion, biliary elimination of many drugs and organic anions such as bilirubin may be impaired (30,43,46) and the concentrations of bile acids reaching the intestine may be inadequate for optimal fat digestion (45). This immaturity of liver function may also place the infant at increased risk for clinical cholestasis as is commonly observed during gram negative infection or during parenteral nutrition (2,8,18). It is our hypothesis that during development, efficient enterohepatic cycling of bile acids may, in part, be limited by immaturity of bile acid transport by the liver. We, therefore, sought maturational changes in the uptake of taurocholate by hepatocytes isolated from suckling and weanling rats.for hepatocyte isolation and all studies were conducted at midday.The chemicals used in this study were: tauro-[~arbonyl-'~C] cholic acid, (52.0 mCi/mmoles; greater than 98% pure by thin layer chromatography) and [3H]-inulin, (1 mCi/6.9 mg) both from New England Nuclear Corp. (Boston, MA); collagenase (type II), Sigma Chemical Corp. (St. Louis, MO); sodium taurocholate (greater than 98% pure ...

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Section: Resultssupporting

confidence: 87%

Section: Discussionsupporting

confidence: 88%

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Uptake of Taurocholate by Hepatocytes Isolated from Developing Rats

Suchy

Balistreri

1982

Pediatr Res

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“…However, this discrepancy can be explained by the existence of a low resistant pathway for transepithelial ions and water between the canalicular lumen and sinusoidal space (10,13,27,34). A recent study demonstrated that the hepatic uptake of bile acids is strongly sodium-dependent, though the membrane carrier for bile acids has not been elucidated (2,12,41). In other words, the sodium gradient maintained by Na-K-ATPase plays a key role in bile acid transport by the liver.…”

Section: Discussionmentioning

confidence: 99%

Cytochemical localization of ouabain-sensitive, K-dependent p-nitrophenylphosphatase in the rat hepatocyte.

Yamamoto

Mayahara

Ogawa

1984

Acta Histochem. Cytochem

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“…It is the only transporter that is involved in uptake of bile salts into hepatocytes. Steroid hormones, thyroid hormones, conjugated drugs also transported along with bile acid through NTCP [1].…”

Section: Sodium Taurocholate Cotransporting Polypeptide (Ntcp)mentioning

confidence: 99%

Deciphering the mystery of hepatitis B virus receptors: A historical perspective

2015

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Hepatitis B virus is one of the major reasons of viral hepatitis with an estimated 350 million infected patients worldwide. Although, the virus was discovered and cloned more than three decades ago, its entry mechanism has still been in investigation. Numerous potential candidates have been proposed and investigated rigorously to reveal HBV entry mechanism and to unveil the first door of viral entry to hepatocytes. This review provides a short account of role of receptors for entry of HBV into hepatocytes. The viral preS1 region of large surface protein is involved in the attachment of HBV to hepatocytes. The putative attachment site of HBV is located at amino acids 21-47 of preS1. So far, several proteins have been proposed to interact with these different regions of the preS1 domain which includes human immunoglobulin A receptor, glyceraldehyde-3-phosphate dehydrogenase, interleukin-6, a 31-kDa protein, HBV binding factor, asialoglycoprotein receptor, nascent polypeptide-associated complex a polypeptide, lipoprotein lipase, hepatocyteassociated heparan sulfate proteoglycans, glucose-regulated protein 75. However, none of them have appeared to be generally accepted as a true receptor for the virus until recently when sodium taurocholate cotransporting polypeptide identified as HBV entry receptor. Current review provides scientific historical perspective of various candidates known to be interacting with preS1 of HBV for their possible role in viral entry.

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Effect of Na⊕ on Bile Acid Uptake by Isolated Rat Hepatocytes

Cited by 44 publications

References 0 publications

Uptake of Taurocholate by Hepatocytes Isolated from Developing Rats

Uptake of Taurocholate by Hepatocytes Isolated from Developing Rats

Cytochemical localization of ouabain-sensitive, K-dependent p-nitrophenylphosphatase in the rat hepatocyte.

Deciphering the mystery of hepatitis B virus receptors: A historical perspective

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