G.S. Tint

Rutgers New Jersey Medical School

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Sarah Shefer

Rutgers New Jersey Medical School

G Salen

East Orange VA Medical Center

A K Batta

Veterans Biomedical Research Institute

Gerald Salen

Rutgers New Jersey Medical School

B. Dayal

Rutgers, The State University of New Jersey

Guorong Xu

Northwest University

Susan Hauser

Veterans Biomedical Research Institute

Larry McNease

Louisiana State University

Sandra K. Erickson

University of California, San Francisco

L B Nguyen

Rutgers New Jersey Medical School

Cooperative Institutions

Rutgers New Jersey Medical School

Veterans Biomedical Research Institute

Rutgers, The State University of New Jersey

East Orange VA Medical Center

University Hospital, Newark

Rockefeller University

University of California, San Diego

University of South Florida

Newark Academy

Cabrini Medical Center

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Cholic acid biosynthesis: conversion of 5p-choles- tan e-3a, 7a, 1 2a ,25-tet ro I i n to 5p-c h o I estan e- 3a,7a,l2a,24p,25=pentol by human and rat liver microsomes

F. W. Cheng Sarah Shefer B. Dayal G.S. Tint Toshiaki Setoguchi

This paper describes the conversion of 5P- cholestane-3a,7a, 12q25-tetrol into 3/3-cholestane-3a,7a, 12a,24P,25-pentol by liver microsomes. A sensitive radio- active assay for measuring the formation of 5P-cholestane- 3a,7a, 12a,24P,25-pentol was developed. Optimal assay conditions for human and rat microsomal systems were established. A higher 24P-hydroxylation activity was detected in rat than in human liver under the conditions employed. The hydroxylation of 5P-cholestane-3a,7a, 12a, 25-tetrol by the rat liver microsomal fraction fortified with NADPH was stimulated about two-fold by administration of phenobarbital. Phenobarbital treatment also stimulated hydroxylations at C-23, C-24a, and C-26. Carbon monoxide markedly inhibited all side-chain hydroxylations. In con- trast, side-chain hydroxylase activities were not affected in animals deprived of food for 48 hr. These results are consistent with a previously postulated cholic acid bio- synthetic pathway involving 5P-cholestane-3a,7a, 12a,24P, 25-pent01 as a key intermediate in man and in the rat.

Cholestane

Hydroxylation

Phenobarbital

Side chain

Source

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Effect of 7-Ketolithocholic Acid on Bile Acid Metabolism in Humans

Gastroenterology (1982)

Gerald Salen Diane Verga A K Batta G.S. Tint Sarah Shefer

Ursodeoxycholic acid

Chenodeoxycholic acid

Lithocholic acid

Deoxycholic acid

10.1016/s0016-5085(82)80326-0

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Citations (18)

Failure of a child with the smith-lemli-opitz syndrome (SLO) to synthesize bile acids: Effect of cholesterol (CH) and bile acid (BA) feeding

Hepatology (1993)

G.S. Tint

Smith–Lemli–Opitz syndrome

10.1016/0270-9139(93)92242-r

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Citations (2)

Regulation of cholesterol 7A-hydroxylase by orphan nuclear receptors in cholesterol-fed and bile fistula rabbits

Gastroenterology (2000)

Guorong Xu Gerald Salen Sandra K. Erickson Sarah Shefer Steve R. Lear

10.1016/s0016-5085(00)82828-0

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Regulation of cholesterol 7 alpha-hydroxylase by hepatic 7 alpha-hydroxylated bile acid flux and newly synthesized cholesterol supply.

Journal of Biological Chemistry (1991)

Sarah Shefer L B Nguyen G Salen G C Ness G.S. Tint

We measured hepatic cholesterol 7 alpha-hydroxylase activity, mass, and catalytic efficiency (activity/unit mass) in bile fistula rats infused intraduodenally with taurocholate and its 7 beta-hydroxy epimer, tauroursocholate, with or without mevalonolactone to supply newly synthesized cholesterol. Enzyme activity was measured by an isotope incorporation assay and enzyme mass by densitometric scanning of immunoblots using rabbit anti-rat liver cholesterol 7 alpha-hydroxylase antisera. Cholesterol 7 alpha-hydroxylase activity increased 6-fold, enzyme mass 34%, and catalytic efficiency 5-fold after interruption of the enterohepatic circulation for 48 h. When taurocholate was infused to the bile acid-depleted animals at a rate equivalent to the hepatic bile acid flux (27 mumol/100-g rat/h), cholesterol 7 alpha-hydroxylase activity and enzyme mass declined 60 and 61%, respectively. Tauroursocholate did not significantly decrease cholesterol 7 alpha-hydroxylase activity, mass and catalytic efficiency. The administration of mevalonolactone, which is converted to cholesterol, modestly increased cholesterol 7 alpha-hydroxylase activity and enzyme mass in the bile acid-depleted rats. However, when taurocholate was infused together with mevalonolactone, cholesterol 7 alpha-hydroxylase activity and catalytic efficiency were markedly depressed while enzyme mass did not change as compared with bile acid-depleted rats. These results show that (a) hepatic bile acid depletion increases bile acid synthesis mainly by activating cholesterol 7 alpha-hydroxylase with only a small rise in enzyme mass, (b) replacement with taurocholate for 24 h decreases both cholesterol 7 alpha-hydroxylase activity and mass proportionally, (c) when cholesterol is available (mevalonolactone supplementation), the infusion of taurocholate results in the formation of a catalytically less active cholesterol 7 alpha-hydroxylase, and (d) tauroursocholate, the 7 beta-hydroxy epimer of taurocholate, does not inhibit cholesterol 7 alpha-hydroxylase. Thus, bile acid synthesis is modulated by the catalytic efficiency and mass of cholesterol 7 alpha-hydroxylase. The enterohepatic flux of 7 alpha-hydroxylated bile acids and the formation of hepatic cholesterol apparently control cholesterol 7 alpha-hydroxylase by different mechanisms.

Enterohepatic circulation

Reverse cholesterol transport

Taurocholic acid

Alpha (finance)

Specific activity

10.1016/s0021-9258(18)49898-5

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Citations (30)

Comparative effects of high and low dose ursodeoxycholic acid on gallstone dissolution and biliary lipid composition

Gastroenterology (1978)

G Salen Anthony Colallilo G.S. Tint Sarah Shefer

Ursodeoxycholic acid

10.5555/uri:pii:0016508578906455

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Citations (2)

Comparative effect of a low sterol diet on cholesterol and bile acid synthesis in a sitosterolemic homozygote and a heterozygote subject

Atherosclerosis (1994)

Margaret M. Cobb G Salen G.S. Tint

Heterozygote advantage

Compound heterozygosity

10.1016/0021-9150(94)93303-0

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Biliary bile acids, bile alcohols, and sterols of Alligator mississippiensis.

Journal of Lipid Research (1980)

G.S. Tint B. Dayal A K Batta Sarah Shefer Ted Joanen

Bile from Alligator mississippiensis was found to contain a mixture of more than twenty bile acids, bile alcohols, and neutral sterols.Bile acids and bile alcohols were purified by reversed-phase high performance liquid chromatography and thin-layer chromatography.Concentrations were measured by gas-liquid chromatography on 1% HiEFF-8BP and identifications were made by mass spectrometry.The major neutral sterols consisted of 98% cholesterol and 0.8% cholestanol.Bile acids recovered from the acidic fraction were 3a,7a,l2a-trihydroxy-5P-cholestanoic acid (61 %), 3a,7a-dihydroxv-5P-cholestanoic acid (9%), 3a,7a, 12a-trihydroxy-5a-cholestanoic acid (8%), and 3-oxo-7a,l2a-dihydroxy-5P-cholestanoic acid (10%).Other C,, bile acids identified were: 3a, 12a-dihydroxy-5P-cholestanoic acid, 7-oxo-3a,l2a-dihydroxy-5P-cholestanoic acid, and 3-oxo-7a, 12a-dihydroxy-5a-cholestanoic acid.Small quantities of C24 cholic, 5a-cholic, chenodeoxycholic, and ursodeoxycholic acids were also detected, as were trace amounts of the CZ7 bile alcohols 5a-cholestane-3a,7a,l2a, 26-tetrol, and 5P-cholestane-3a,7a, 12a,25-tetrol.These results suggest that the alligator is capable of synthesizing both the 5a and 5P-isomers of the Cq7 bile acids.T h e small amounts of the C,, bile acids present might originate either from C,, bile acid or bile alcohol precursors or from exogenous sources.-

American alligator

Cholestanol

10.1016/s0022-2275(20)39844-8

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Citations (33)

Ursodeoxycholic acid (UDCA) reduces elevated plasma endogenous bile acids following orthotopic liver transplant

Hepatology (1993)

G.S. Tint

Ursodeoxycholic acid

10.1016/0270-9139(93)92901-b

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