Bile Acids Inhibit Secretion of Very Low Density Lipoprotein by Rat Hepatocytes

Pozo, Reginald Del; Barth, C. A.

doi:10.1515/bchm3.1987.368.2.887

Cited by 9 publications

(6 citation statements)

References 1 publication

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“…Net accumulation of perfusate VLDL cholesterol and triglyceride was decreased alter perfusion with either bile salt. This observation is consistent with that reported by Del Pozo and Barth (20) who observed decreased VLDL secretion by isolated rat hepatocytes exposed to bile salts. The ratio of free to esterified cholesterol in VLDL was unchanged by bile salt perfusion; free cholesterol was about 70% of the total in all samples.…”

Section: Resultssupporting

confidence: 93%

Effects of bile salts on rat hepatic acyl CoA:Cholesterol acyltransferase

Erickson

Zuiden

1995

Lipids

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Acyl CoA:cholesterol acyltransferase (EC2.3.1.26, ACAT), responsible for intracellular esterification of cholesterol, may play an important role in cholesterol trafficking within the cell, and thus, in maintenance of cellular cholesterol homeostasis. Bile acids are potential regulators of cholesterol trafficking in the liver. Therefore, the effect of bile salts on hepatic ACAT activity was studied in the perfused rat liver. ACAT activity was increased after liver perfusion with either taurocholate or taurochenodeoxycholate. However, addition of these bile salts at physiological concentrations in vitro had little effect on microsomal ACAT activity. The increase in hepatic ACAT activity due to perfusion with bile salts was accompanied by reduced accumulation of very low density lipoprotein cholesterol in the perfusate, but there was no effect on 3-hydroxy-3-methylglutaryl-CoA reductase activity. Hepatic ACAT activity was decreased after bile diversion for four hours in the intact animal. This treatment had no statistically significant effect on 3-hydroxy-3-methylglutaryl-CoA reductase activity. These data suggest that bile salts induce changes in hepatic compartmentation and traffic of cholesterol within the hepatocyte accompanied by response of ACAT activity to maintain cellular cholesterol homeostasis.

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Section: Resultssupporting

confidence: 93%

Effects of bile salts on rat hepatic acyl CoA:Cholesterol acyltransferase

Erickson

Zuiden

1995

Lipids

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“…These studies provide the first description in the live animal of the various alterations in TG metabolism that result from XGB in the mouse. Contrariwise to our hypothesis that the increased flux of BA after XGB would decrease serum TG and hepatic VLDL through the inhibitory effects of BA on VLDL–TG production (35–37), we surprisingly found increased serum and hepatic TG levels, increased hepatic VLDL production and increased hepatic MTTP activity in XGB mice.…”

Section: Discussionsupporting

confidence: 66%

“…Because BA circulates faster after XGB, the increased flux of BA molecules per unit time could activate a number of cell signalling processes and modify metabolic regulation during the feed/fast cycle [reviewed in (16–20)]. One of these metabolic changes could be a decrease in serum and hepatic TG levels through the inhibitory effects of BA on VLDL–TG production (35–37). Alternatively, the abrogation of the GB, as a source of FGF15/19 (21) and of the membrane‐bound BA receptor TGR5 (40) that also has important effects on metabolic homoeostasis (41), could also affect TG metabolism.…”

mentioning

confidence: 99%

Cholecystectomy increases hepatic triglyceride content and very‐low‐density lipoproteins production in mice

Amigo

Husche

Zanlungo

et al. 2010

Liver International

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“…Furthermore, when compared with normal subjects, hypertriglyceridemic patients have a decreased level of the ileal sodium bile acid transporter, resulting in an impaired enterohepatic recycling of bile acids (40). Finally, addition of bile acids to cultured rat and human hepatocytes decreased VLDL secretion (41)(42)(43), underscoring the crucial role of the liver in this process.…”

Section: Discussionmentioning

confidence: 91%

Bile acids lower triglyceride levels via a pathway involving FXR, SHP, and SREBP-1c

Watanabe¹,

Wang²,

Moschetta³

et al. 2004

J. Clin. Invest.

288

324

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We explored the effects of bile acids on triglyceride (TG) homeostasis using a combination of molecular, cellular, and animal models. Cholic acid (CA) prevents hepatic TG accumulation, VLDL secretion, and elevated serum TG in mouse models of hypertriglyceridemia. At the molecular level, CA decreases hepatic expression of SREBP-1c and its lipogenic target genes. Through the use of mouse mutants for the short heterodimer partner (SHP) and liver X receptor (LXR) α and β, we demonstrate the critical dependence of the reduction of SREBP-1c expression by either natural or synthetic farnesoid X receptor (FXR) agonists on both SHP and LXRα and LXRβ. These results suggest that strategies aimed at increasing FXR activity and the repressive effects of SHP should be explored to correct hypertriglyceridemia. 1408The Nonstandard abbreviations used: acetyl-CoA carboxylase (ACC); acetyl-CoA synthetase (AceCS); angiopoietin-like protein 3 (ANGPTL3); carnitine palmitoyltransferase I (CPT-I); chenodeoxycholic acid (CDCA); cholesterol 7α-hydroxylase (CYP7A1); cholic acid (CA); farnesoid X receptor (FXR); fatty acid synthase (FAS); LDL receptor (LDL-R); liver receptor homolog-1 (LRH-1); liver receptor homolog-1 response element (LRH-1RE); liver X receptor (LXR); liver X receptor response element (LXRRE); long-chain acyl-CoA dehydrogenase (LCAD); malic enzyme (ME); medium-chain acyl-CoA dehydrogenase (MCAD); retinoid X receptor (RXR); short heterodimer partner (SHP); stearoyl-CoA desaturase-1 (SCD-1); triglyceride (TG). Conflict of interest:The authors have declared that no conflict of interest exists. Plasmids. pCMX-SHP was obtained by insertion of a PCR product corresponding to the mouse SHP cDNA into the pCMX vector. pCMX-liver receptor homolog-1 (pCMX-LRH-1) was produced by insertion of a PCR product corresponding to the mouse LRH-1 cDNA into pCMX. The pCMX-LXRα expression vector was as described (10); the pSG5-retinoid X receptor α (pSG5-RXRα) expression vector was a gift of P. Chambon (Institut Clinique de la Souris, Illkirch, France). The SREBP-1c promoter luciferase reporter plasmids were generated by PCR amplification of promoter fragments corresponding to sequences located between -1070 to -51 of the mouse SREBP-1c gene. The PCR product was ligated into the pGL3 basic vector (Promega, Madison, Wisconsin, USA). The reverse primer used for each promoter construct is 5′-CTTCCGCGCCGATTTCACCTG-3′. The different forward primers used for each construct are as follows: pSREBP-1c1070-Luc (5′-ACCCCTCAGACTGTGTGAGT-3′), pSREBP-1c571-Luc (5′-CTA GCTAGATGACCCTGCACCACCAA-3′), pSREBP-1c327-Luc (5′-TTGCCTGTGCGGCAGGGGTTGGGACGA-3′), pSREBP1c276-Luc (5′-CGCGCTGGCGCAGACGCGGTTAAA-3′), and pSREBP-1c151-Luc (5′-CTGCTGATTGGCCATGTGCGCTCA-3′). The primers were tailed with either a KpnI site (forward) or a BglII site (reverse). The LXR response elements in pSREBP-1c324-Luc were mutated for promoter analysis using the Quick Change SiteDirected Mutagenesis Kit (Stratagene, La Jolla, California, USA). All constructs were verified by sequence analysis.Ani...

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Bile Acids Inhibit Secretion of Very Low Density Lipoprotein by Rat Hepatocytes

Cited by 9 publications

References 1 publication

Effects of bile salts on rat hepatic acyl CoA:Cholesterol acyltransferase

Effects of bile salts on rat hepatic acyl CoA:Cholesterol acyltransferase

Cholecystectomy increases hepatic triglyceride content and very‐low‐density lipoproteins production in mice

Bile acids lower triglyceride levels via a pathway involving FXR, SHP, and SREBP-1c

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