Interruption Of Enterohepatic Circulation Research Articles

Roles for Bile Acid Signaling and Nonsense-Mediated Ribonucleic Acid Decay in Small Bowel Resection-Associated Liver Injury

IntroductionMassive intestinal loss resulting in short bowel syndrome has been linked to intestinal failure associated liver disease. Efforts to elucidate the driving force behind the observed hepatic injury have identified inflammatory mediators, alterations in the microbiome, extent of structural and functional intestinal adaptation, and toxic shifts in the bile acid pool. In the present study, we posit that ileocecal resection interrupts the delivery of these hepatotoxic substances to the liver by physically disrupting the enterohepatic circulation, thereby shielding the liver from exposure to the aforementioned noxious stimuli. MethodsMice underwent sham, 50% proximal, or 50% distal small bowel resection (SBR), with or without tauroursodeoxycolic acid supplementation. Enterohepatic signaling and nonsense-mediated ribonucleic acid (RNA) decay were evaluated and correlated with hepatic injury. ResultsWhen compared to 50% proximal SBR, mice that underwent ileocecal resection exhibited reduced hepatic oxidative stress and exhibited a more physiological bile acid profile with increased de novo bile acid synthesis, enhanced colonic bile acid signaling, and reduced hepatic proliferation. Distal intestinal resection promoted an adaptive response including via the nonsense-mediated RNA decay pathway to satisfactorily process injurious messenger RNA and successfully maintain homeostasis. By contrast, this adaptive response was not observed in the proximal SBR group and hepatic injury persisted. ConclusionsIn summary, interruption of enterohepatic circulation via ileocecal resection abrogates the liver's exposure to toxic and inflammatory mediators while promoting physiological adaptations in bile acid metabolism and maintaining existing homeostatic pathways.

Diseases Producing Malabsorption and Maldigestion

Malabsorption refers to the impaired intestinal absorption of nutrients. It can result from congenital defects in absorption and the transport of ions and nutrients, defects in hydrolysis within the intestinal lumen, acquired defects in the intestinal absorptive cells that line the surface of the intestine, impaired bile production, or interruption of enterohepatic circulation or secondary to pancreatic insufficiency. Maldigestion, another factor in nutrient absorption, refers to the impaired digestion of nutrients within the intestinal lumen or at the terminal digestive site of the brush border membrane of mucosal epithelial cells. Although malabsorption and maldigestion are pathophysiologically distinct, they are interdependent, and in clinical practice, malabsorption has come to signify derangements in either or both processes. This chapter discusses the clinical manifestations of malabsorption and tests for suspected malabsorption. The diseases that can cause malabsorption, their diagnosis, and treatment recommendations are included. Figures illustrate the diagnosis and management of celiac disease; an approach to gluten challenge for the diagnosis or exclusion of celiac disease in patients maintained on a gluten-free diet without previous definitive diagnostic testing; and the histologic features of celiac disease, Crohn disease, collagenous sprue, autoimmune enteropathy, eosinophilic gastritis, and intestinal lymphangiectasia. This review contains 9 figures, 25 tables, and 116 references. Keywords: Malabsorption, maldigestion, Crohn disease, celiac disease, tropical sprue, diarrhea, endoscopy, short bowel syndrome, bacterial overgrowth

Diseases Producing Malabsorption and Maldigestion

Malabsorption refers to the impaired intestinal absorption of nutrients. It can result from congenital defects in absorption and the transport of ions and nutrients, defects in hydrolysis within the intestinal lumen, acquired defects in the intestinal absorptive cells that line the surface of the intestine, impaired bile production, or interruption of enterohepatic circulation or secondary to pancreatic insufficiency. Maldigestion, another factor in nutrient absorption, refers to the impaired digestion of nutrients within the intestinal lumen or at the terminal digestive site of the brush border membrane of mucosal epithelial cells. Although malabsorption and maldigestion are pathophysiologically distinct, they are interdependent, and in clinical practice, malabsorption has come to signify derangements in either or both processes. This chapter discusses the clinical manifestations of malabsorption and tests for suspected malabsorption. The diseases that can cause malabsorption, their diagnosis, and treatment recommendations are included. Figures illustrate the diagnosis and management of celiac disease; an approach to gluten challenge for the diagnosis or exclusion of celiac disease in patients maintained on a gluten-free diet without previous definitive diagnostic testing; and the histologic features of celiac disease, Crohn disease, collagenous sprue, autoimmune enteropathy, eosinophilic gastritis, and intestinal lymphangiectasia. This review contains 9 figures, 25 tables, and 116 references. Keywords: Malabsorption, maldigestion, Crohn disease, celiac disease, tropical sprue, diarrhea, endoscopy, short bowel syndrome, bacterial overgrowth

ГІПОХОЛЕСТЕРОЛЕМІЧНА ДІЯ N–АЛКІЛАМІДОВАНОГО АЛЬГІНАТУ

It is known that in the process of digestion and absorption of nutrients, one of the key roles belongs to polysaccharides (among which there are alginic acid), which have the ability to increase viscosity and form a gel in the intestine. Previously, we studied the physiological effects of pectin, cellulose and their amidated derivatives that have demonstrated growth of hypocholesterolemic activity in the rats. From here, it was decided to investigate the hypocholesterolemic effect of N–alkylamidated alginate on laboratory animals. That’s why, female rats were fed according to three diets, namely the control (1) and two experimental (2 and 3), which contained cholesterol (10 g/kg) and different amounts N–alkylamidated alginate (0 and 40 g / kg, respectively), and all animals fed also palm oil. N–alkylamidated alginate significantly lowered the level of cholesterol (total and LDL) in serum and liver and of hepatic total lipids in the rats, which were on cholesterol–containing diet. In the faeces of animals that consumed N–alkylamidated alginate, it was observed increased concentrations of fat from 61 to 91 mg / g, while the concentration of cholesterol, bile acids and total sterols was not significantly changed.Hence, decrease cholesterolemia in rats (that consumed N–alkylamidated alginate) is probably based more on the removal of fat from the intestine, rather than on the interruption of enterohepatic circulation of cholesterol.

Nonabsorbable Dietary Fat Enhances Disposal of 2,2‘,4,4‘-Tetrabromodiphenyl Ether in Rats through Interruption of Enterohepatic Circulation

Polybrominated diphenyl ethers are lipophilic persistent organic pollutants (POPs), which accumulate in the environment, leading to human exposure. The compounds exert a negative impact on human health. Strategies to prevent or diminish their accumulation in humans are required. We investigated in rats whether the disposal rate of 14C-labeled tetrabromodiphenyl ether (BDE-47) could be enhanced by increasing fecal fat excretion through dietary treatment with nonabsorbable fat (sucrose polyester, SPE). As compared to control rats, SPE treatment increased fecal excretion rates of fat (+188%, p < 0.05) and 14C-BDE-47 (+291%, p < 0.05). On the basis of biliary secretion and fecal excretion rates of 14C-BDE-47, SPE effectively inhibited the enterohepatic circulation of 14C-BDE-47. In conclusion, dietary supplementation of nonabsorbable fat can enhance excretion of hydrophobic POPs by interruption of their enterohepatic circulation. Our data indicate that this strategy could decrease concentrations of hydrophobic POPs in the human body and thereby their impact on human health.

Studies on adsorption characteristics of bile acids and methotrexate to a new type of anion-exchange resin, colestimide.

The adsorption characteristics of various bile acids and methotrexate to a new type of anion-exchange resin, colestimide, were studied in vitro and compared with those to cholestyramine. For bile acids, colestimide was shown to have a higher capacity than cholestyramine. For example, approximately 1.4-fold higher for cholic acid and 2.0-fold for deoxycholic acid in water. In the presence of physiological anions, the degree of adsorption of cholic acid to both resins was greatly reduced, whereas adsorption of deoxycholic acid was only slightly reduced. Furthermore, the bed-volume of colestimide swelled about 6.8-fold in water, hence the anion-exchange groups of this resin are expected to be able to function effectively in adsorption of bile acids in the gut. In addition, colestimide was found to have high adsorption capacity for methotrexate, not only in water but also in media containing various physiological anions, and thus it is suggested that colestimide is a potential oral antidote to reduce possible toxicity by methotrexate through interruption of enterohepatic circulation.

Simultaneous blood and biliary sampling of esculetin by microdialysis in the rat

Biliary excretion and intestinal reabsorption in enterohepatic circulation play major dispositional roles for some drugs. To circumvent multiple blood sampling and interruption of enterohepatic circulation in conventional biliary cannulation, the present study utilized the minimally invasive sampling technique of microdialysis in pharmacokinetics and biliary excretion studies. Microdialysis probes were inserted into the jugular vein and bile duct in the anesthetized rat for simultaneous and continuous sampling following intravenous administration of esculetin, a bioactive coumarin derivative. Placements of the microdialysis probes were designed to minimize obstruction to normal flows of the body fluids. Separation and quantitation of esculetin in the dialysates were achieved using high performance liquid chromatography (HPLC) coupled to UV detection. The results indicated higher drug concentrations in the bile than in the blood, suggesting active biliary excretion. The study also provided an example of successful application of in vivo microdialysis as an interesting and feasible alternative for pharmacokinetics and biliary drug excretion studies.

Choosing the right lipid-regulating agent. A guide to selection.

If dietary therapy and other lifestyle changes do not adequately normalise blood lipid levels, lipid-regulating drugs, as single-drug or combination-drug therapy, may be prescribed to supplement lifestyle changes. Evaluation of the individual patient's health and risk status, determination of the dyslipidaemia, definition of treatment goals and a clear understanding of the mechanisms and effects of lipid-regulating agents are necessary for optimisation of treatment. Although all the available lipid-regulating agents lower low density lipoprotein (LDL) cholesterol, the agents with the greatest LDL cholesterol-lowering effect are the bile acid sequestrants, which up-regulate the LDL receptor by the decrease in intrahepatic cholesterol caused by the interruption of enterohepatic circulation of cholesterol-rich bile acids, and the HMG-CoA reductase inhibitors, which partially inhibit HMG-CoA reductase. The agents with the greatest triglyceride-lowering effect are nicotinic acid, which decreases the production of very low density lipoprotein (VLDL) cholesterol and reduces the availability of free fatty acids in the circulation, and the fibric acid derivatives, which increase lipoprotein lipase activity and may also decrease the release of free fatty acids. Although the safety profile of the available lipid-regulating drugs has been established, patients should be monitored for potential adverse effects and interactions with concomitantly administered agents. When used correctly, lipid-regulating drug therapy is highly effective in the treatment of a variety of dyslipidaemias.

Effects of interruption of enterohepatic circulation on biliary lipid secretion in man.

To delineate relationships between biliary outputs of bile acids, phospholipids, and cholesterol, studies were carried out in 18 subjects with intact gallbladders and in six with cholecystectomy. Hepatic secretions of three biliary lipids were determined using an intestinal perfusion technique. In studies on subjects with normal gallbladders (study A), continuous infusion of liquid formula was given to stimulate gallbladder contraction, so that gallbladder storage was eliminated and duodenal outputs were equal to hepatic secretion rates. Bile acid pool size and bile lipid outputs were determined under steady-state conditions (intact EHC). Secretion rates of bile acids were then reduced by progressively withdrawing large amounts of bile from the EHC over a 12-hr period, during which biliary lipid secretions were measured continuously. In study B, six subjects without gallbladders ingested three meals of liquid formula during the day and had an overnight fast. Measurements of biliary lipid outputs were made hourly over the 24-hr period. A wide range of bile acid secretion rates occurred under these physiological conditions owing to the lowering of bile acid outputs during fasting. In both studies A and B, bile saturation with cholesterol increased as EHC became interrupted. However, the magnitude of this increase was variable from subject to subject and appeared to depend on two related factors. First, bile saturation was markedly increased in subjects who exhibited a severe reduction of bile acid output on interrupting the EHC. Second, the degree of uncoupling of cholesterol and phospholipid secretion in the lower range of bile acid outputs was also variable. When secretion of cholesterol was well-maintained in the face of decreasing bile acid and phospholipid outputs, bile became supersaturated. Subjects with high biliary cholesterol during intact EHC were especially prone to cholesterol-phospholipid dissociation. However, even at relatively low outputs of cholesterol, interruption of the EHC sometimes caused marked dissociation of secretions of cholesterol and phospholipids causing super-saturated bile at low rates of bile acid flux. Thus, the degree of coupling of cholesterol and phospholipids at low secretion of bile acids was variable from patient to patient and was a major determinant of the extent of increase in bile saturation.

Bile-salt-dependent and independent choleresis induced by bucolome in the rat.

Choleresis induced by bucolome (BC) (1-cyclohexyl-5-n-butyl-2,4,6-trioxoperhydropyrimidine) was studied in male Wistar rats. [14C]Erythritol and mannitol clearance studies indicated this choleresis to be of canalicular origin. In 1-h continuous bile collection studies, immediately after the interruption of enterohepatic circulation (acute interruption), both bile flow and bile salt excretion rates were significantly increased in rats administered BC. However, the bile salt excretion rate fell rather rapidly in BC-administered rats, while the bile flow rate was fairly constant during this 1-h period. Thus, unlike the situation in control rats, bile flow rate was not significantly correlated with the bile salt excretion rate in BC-administered rats. In rats that had an external bile fistula open for 16-20 h (chronic interruption of enterohepatic circulation) the bile flow rate was also significantly increased by BC administration, while the bile salt excretion rate was not changed after BC administration. It is suggested that BC induced bile-salt-independent choleresis in both experimental rat groups (acute and chronic interruption of enterohepatic circulation). In addition, BC appeared to increase the bile-salt-dependent fraction of bile in rats with acute interruption of enterohepatic circulation, possibly by mobilizing the bile salt pooled in the intestinal content and (or) intestinal wall.

Effects of meals and interruption of enterohepatic circulation on flow, lipid composition, and cholesterol saturation of bile in man after cholecystectomy.

In 4 patients studied after cholecystectomy and common-duct exploration for cholesterol gallstones, bile salt (BS) and phospholipid (PL) output and bile flow increased significantly in response to breakfast, but cholesterol (Ch) output was unaltered. Simultaneously, Ch concentration decreased while PL and BS concentrations did not change. The degree of Ch saturation of bile, [BS PLUS PL]/[ch], decreased in each study, whether or not the original ratio indicated Ch supersaturation; in 3 of 5 studies, an initially super-saturated bile became unsaturated with Ch in response to breakfast. No significant changes were noted after lunch. During interruption of enterohepatic circulation (EHC), studies with radiolabeled bile acids indicated that the increased bile acid output in response to meals was secondary to increased recirculation of intestinal bile acids rather than to de novo bile acid synthesis. This mechanism may account for the adequate delivery of BS and for the decreased degree of Ch saturation of bile postprandially in cholecystectomized patients.

SMALL-INTESTINAL INJURY IN WOMEN WHO HAVE HAD PELVIC RADIOTHERAPY

17 women who had had radiotherapy for pelvic malignancy were studied. 12 of them had noted a permanent change in their bowel habit, ranging from abandonment of the use of laxatives to frequent bouts of diarrhœa necessitating a change in life-style. 16 of 17 patients had abnormal cholyl-glycine-1-[ 14C] breath tests, including all 12 with symptoms. 8 of the 11 small-bowel X-rays were abnormal, but only 1 of 13 rectal biopsies showed changes of inflammation and another showed vascular thickening, which is regarded as characteristic of radiation damage to the gut. No subject had noted blood in her stools. It is concluded that the alteration in stool habit and the interruption of enterohepatic circulation are caused by radiation injury to the small bowel and that such injury is an almost invariable accompaniment to all forms of pelvic radiotherapy.

Biliary excretion of lecithin and cholesterol in the dog.

The biliary excretion rates of bile acid, lecithin, and cholesterol were measured in unanesthetized dogs after interruption of enterohepatic circulation and during infusions of sodium taurocholate, sodium glycocholate, sodium dehydrocholate, SC2644 (a bicyclic organic acid with high choleretic potency), and secretin. Both lecithin output and cholesterol output were directly related to bile acid excretion rate. The curves describing these relationships were concave downward. Molar concentration ratios of lecithin-to-bile acid declined gradually from approximately 0.4 to 0.2 as bile acid output increased from approximately 1 to 70 mumoles/min. Cholesterol-to-lecithin molar ratios were highest (0.05-0.15) at very low rates of bile acid excretion, but descended rapidly to a plateau (0.03-0.04) which was constant over the entire range of bile acid excretion rates from 10 to 70 mumoles/min. Similar lipid excretion patterns were observed during glycocholate infusion, but secretin-induced choleresis and dehydrocholate-induced choleresis were unaccompanied by any increments in lecithin or cholesterol excretion and SC2644 (which caused a marked increase in canalicular bile production as measured by erythritol clearance) caused a depression of lipid excretion. The data are consistent with the view that lecithin moves passively from cell membranes to intracanalicular micelles, that transport of cholesterol is coupled to lecithin transport, and that there is also a small amount of independent passive transport of cholesterol from membranes to micelles. A model developed on these assumptions has been shown to behave in a fashion consistent with the entire range of these observations.

Canalicular bile production in dogs.

Canalicular bile production in dogs.

Ileal bile salt transport: mutual inhibition in an in vivo system.

ARTICLESIleal bile salt transport: mutual inhibition in an in vivo systemKW Heaton, and L LackKW Heaton, and L LackPublished Online:01 Mar 1968https://doi.org/10.1152/ajplegacy.1968.214.3.585MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByDrug Transport and Membrane Transport Proteins15 September 2010Membrane Transport Proteins and Drug Transport15 January 2003Modeling of active transport systemsAdvanced Drug Delivery Reviews, Vol. 54, No. 3STRUCTURAL BIOLOGY AND FUNCTION OF SOLUTE TRANSPORTERS: IMPLICATIONS FOR IDENTIFYING AND DESIGNING SUBSTRATES27 November 2002 | Drug Metabolism Reviews, Vol. 34, No. 4Effect of Chronic Administration of Tauro-hyodeoxycholic Acid on Biliary Bile Acid Composition and on Biliary Lipid Secretion in Humans8 July 2009 | Scandinavian Journal of Gastroenterology, Vol. 36, No. 9Use of the intestinal and hepatic bile acid transporters for drug deliveryAdvanced Drug Delivery Reviews, Vol. 20, No. 1Intestinal Transport of Bile Acids1 January 2011Active absorption of conjugated bile acids in vivoGastroenterology, Vol. 100, No. 1Effect of chronic administration of ursodeoxycholic acid on the ileal absorption of endogenous bile acids in manHepatology, Vol. 12, No. 5Serum Bile AcidsUtilizing Bile Acid Carrier Mechanisms to Enhance Liver and Small Intestine AbsorptionAnnals of the New York Academy of Sciences, Vol. 507, No. 1 Biological ApIleal absorption of tyrosine-conjugated bile acids in Wistar ratsBiochimica et Biophysica Acta (BBA) - General Subjects, Vol. 926, No. 2Simulation of the metabolism and enterohepatic circulation of endogenous deoxycholic acid in humans using a physiologic pharmacokinetic model for bile acid metabolismGastroenterology, Vol. 93, No. 4Simulation of the metabolism and enterohepatic circulation of endogenous chenodeoxycholic acid in man using a physiological pharmacokinetic modelEuropean Journal of Clinical Investigation, Vol. 16, No. 5Kinetics of Taurocholate Uptake by Isolated Ileal Cells of Guinea PigEuropean Journal of Biochemistry, Vol. 131, No. 2Resorption von GallensäurenBile acid uptake by isolated intestinal mucosa cells of guinea pigBiochimica et Biophysica Acta (BBA) - Molecular Cell Research, Vol. 721, No. 3Properties and biological significance of the ileal bile salt transport system.Environmental Health Perspectives, Vol. 33Pathophysiology of the enterohepatic circulation of bile acids21 June 2005Bile Salt Metabolism:I. The Physiology of Bile Salts25 March 2008 | Australian and New Zealand Journal of Medicine, Vol. 7, No. 6Interaction of uncharged bile salt derivatives with the ileal bile salt transport systemJournal of Lipid Research, Vol. 18, No. 3Dynamics of the Enterohepatic Circulation of the Glycine Conjugates of Cholic, Chenodeoxycholic, Deoxycholic, and Sulfolithocholic Acid in ManGastroenterology, Vol. 72, No. 3Ionic requirements for the active ileal bile salt transport systemJournal of Lipid Research, Vol. 17, No. 6Regional Ileitis (Crohn’s Disease)16 October 2020 | Scandinavian Journal of Gastroenterology, Vol. 11, No. 5Characterization of the passive and active transport mechanisms for bile acid uptake into rat isolated intestinal epithelial cellsBiochimica et Biophysica Acta (BBA) - Biomembranes, Vol. 406, No. 2Interactions of cationic bile salt derivatives with the ileal bile salt transport system.Journal of Lipid Research, Vol. 16, No. 5Effects of meals and interruption of enterohepatic circulation on flow, lipid composition, and cholesterol saturation of bile in man after cholecystectomyThe American Journal of Digestive Diseases, Vol. 20, No. 2Effect of Phenobarbital on Intestinal Cholic Acid Absorption in the RatGastroenterology, Vol. 67, No. 6Bile Salt Transport SystemsIleal transport of bile acids conjugated with norleucine and lysineBiochimica et Biophysica Acta (BBA) - Biomembranes, Vol. 266, No. 1Transport of DrugsThe Enterohepatic CirculationGastroenterology, Vol. 62, No. 1Metabolism and transport of bile salts in the intestineThe American Journal of Medicine, Vol. 51, No. 5Changes in Fat Absorption following small Bowel Resection in the Dog27 September 2008 | Archives Internationales de Physiologie et de Biochimie, Vol. 79, No. 5Morphological changes of the small-intestinal mucosa of guinea pig and hamster following incubation in vitro and perfusion in vivo with unconjugated bile saltsGut, Vol. 11, No. 6Effects of Sulfation of Taurolithocholic and Glycolithocholic Acids on their Intestinal TransportGastroenterology, Vol. 56, No. 4 More from this issue > Volume 214Issue 3March 1968Pages 585-590 Copyright & PermissionsCopyright © 1968 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1968.214.3.585PubMed5644097History Published online 1 March 1968 Published in print 1 March 1968 Metrics

Role of pyloric antrum in choleresis after insulin and feeding.

ARTICLESRole of pyloric antrum in choleresis after insulin and feedingRS Jones, and FP BrooksRS Jones, and FP BrooksPublished Online:01 Dec 1967https://doi.org/10.1152/ajplegacy.1967.213.6.1406MoreSectionsPDF (554 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByEffect of verapamil on insulin-stimulated choleresisJournal of Surgical Research, Vol. 49, No. 1Enhancement by Secretin of the Apparently Maximal Hepatic Transport of Bilirubin in the RatHepatology, Vol. 4, No. 4Effect of secretin, pancreozymin OP-CCK, and glucagon on bile flow and bile lipid secretion in rats.Gut, Vol. 24, No. 9Effects of meals and interruption of enterohepatic circulation on flow, lipid composition, and cholesterol saturation of bile in man after cholecystectomyThe American Journal of Digestive Diseases, Vol. 20, No. 2SIGNIFICANCE OF METABOLIC DISORDERS IN SCHIZOPHRENIAThe Lancet, Vol. 301, No. 7806ALTERED ABSORPTION OF DIGOXIN IN PATIENTS GIVEN PROPANTHELINE AND METOCLOPRAMIDEThe Lancet, Vol. 301, No. 7806Secretin and Cholecystokinin (CCK)Bile SecretionClinics in Gastroenterology, Vol. 2, No. 1Effect of Selective and Truncal Vagotomy on Insulin-Stimulated Bile Secretion in DogsGastroenterology, Vol. 60, No. 4Comparison of Dose–Response Relations of Insulin and 2-Deoxy-D-Glucose for Biliary and Gastric Acid Secretion in DogsGastroenterology, Vol. 59, No. 5The secretion of bileThe American Journal of Digestive Diseases, Vol. 14, No. 5 More from this issue > Volume 213Issue 6December 1967Pages 1406-1408 Copyright & PermissionsCopyright © 1967 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1967.213.6.1406PubMed6075741History Published online 1 December 1967 Published in print 1 December 1967 Metrics

Interruption of enterohepatic circulation of bile and its effect on the urinary and biliary excretion of I-131

Interruption of enterohepatic circulation of bile and its effect on the urinary and biliary excretion of I-131

Regulation of cholesterol oxidation by liver in vitro.

SummaryA feedback mechanism, whereby conjugated bile acids control oxidation of cholesterol in liver, has been discerned in vitro. Addition of cholic acid conjugates depressed oxidation of cholesterol, but not that of sodium pyruvate or 3a, 7a, 12a-trihydroco-prostane, by fortified rat liver mitochondrial preparations. Preparations from livers of rats, deprived of bile salts by interruption of enterohepatic circulation, oxidized cholesterol to a greater extent than controls. The site of action of the feedback effect is discussed briefly.