scholarly journals Monoglyceride lipase deficiency affects hepatic cholesterol metabolism and lipid-dependent gut transit in ApoE−/− mice

Oncotarget ◽  
2017 ◽  
Vol 8 (20) ◽  
pp. 33122-33136 ◽  
Author(s):  
Nemanja Vujic ◽  
Melanie Korbelius ◽  
Christina Leopold ◽  
Madalina Duta-Mare ◽  
Silvia Rainer ◽  
...  
Keyword(s):  
Cholesterol Metabolism ◽  
Hepatic Cholesterol ◽  
Monoglyceride Lipase

scholarly journals Hepatic cholesterol metabolism in cholesterol gallstone disease

1991 ◽  
Vol 32 (3) ◽  
pp. 469-475
Author(s):  
E Reihnér ◽  
B Angelin ◽  
I Björkhem ◽  
K Einarsson
Keyword(s):  
Cholesterol Metabolism ◽  
Cholesterol Gallstone ◽  
Gallstone Disease ◽  
Hepatic Cholesterol

scholarly journals Hepatic cholesterol metabolism in normo- and hyperlipidemic patients with cholesterol gallstones.

1979 ◽  
Vol 20 (1) ◽  
pp. 107-115
Author(s):  
J Ahlberg ◽  
B Angelin ◽  
I Björkhem ◽  
K Einarsson ◽  
B Leijd
Keyword(s):  
Cholesterol Metabolism ◽  
Hepatic Cholesterol ◽  
Cholesterol Gallstones

scholarly journals Short- and long-term effects of biliary drainage on hepatic cholesterol metabolism in the rat

1990 ◽  
Vol 269 (3) ◽  
pp. 781-788 ◽  
Author(s):  
M J Smit ◽  
A M Temmerman ◽  
R Havinga ◽  
F Kuipers ◽  
R J Vonk
Keyword(s):  
Bile Acid ◽  
Bile Flow ◽  
Cholesterol Metabolism ◽  
Acid Output ◽  
Biliary Secretion ◽  
Surgical Trauma ◽  
Hepatic Cholesterol ◽  
Long Term Effects ◽  
Short And Long Term

The present study concerns short- and long-term effects of interruption of the enterohepatic circulation (EHC) on hepatic cholesterol metabolism and biliary secretion in rats. For this purpose, we employed a technique that allows reversible interruption of the EHC, during normal feeding conditions, and excludes effects of anaesthesia and surgical trauma. [3H]Cholesteryl oleate-labelled human low-density lipoprotein (LDL) was injected intravenously in rats with (1) chronically (8 days) interrupted EHC, (2) interrupted EHC at the time of LDL injection and (3) intact EHC. During the first 3 h after interruption of the EHC, bile flow decreased to 50% and biliary bile acid, phospholipid and cholesterol secretion to 5%, 11% and 19% of their initial values respectively. After 8 days of bile diversion, biliary cholesterol output and bile flow were at that same level, but bile acid output was increased 2-3-fold and phospholipid output was about 2 times lower. The total amount of cholesterol in the liver decreased after interruption of the EHC, which was mainly due to a decrease in the amount of cholesteryl ester. Plasma disappearance of LDL was not affected by interruption of the EHC. Biliary secretion of LDL-derived radioactivity occurred 2-4 times faster in chronically interrupted rats as compared with the excretion immediately after interruption of the EHC. Radioactivity was mainly in the form of bile acids under both conditions. This study demonstrates the very rapid changes that occur in cholesterol metabolism and biliary lipid composition after interruption of the EHC. These changes must be taken into account in studies concerning hepatic metabolism of lipoprotein cholesterol and subsequent secretion into bile.

The influence of estrogen on hepatic cholesterol metabolism and biliary lipid secretion in rats fed fish oil

1999 ◽  
Vol 1437 (3) ◽  
pp. 367-377 ◽  
Author(s):  
Elena Bravo ◽  
Alfredo Cantafora ◽  
Carla Cicchini ◽  
Michael Avella ◽  
Kathleen M. Botham
Keyword(s):  
Fish Oil ◽  
Cholesterol Metabolism ◽  
Biliary Lipid ◽  
Hepatic Cholesterol ◽  
Lipid Secretion

scholarly journals Disruption of the Sterol Carrier Protein 2 Gene in Mice Impairs Biliary Lipid and Hepatic Cholesterol Metabolism

2001 ◽  
Vol 276 (51) ◽  
pp. 48058-48065 ◽  
Author(s):  
Michael Fuchs ◽  
Andrea Hafer ◽  
Christian Münch ◽  
Frank Kannenberg ◽  
Sandra Teichmann ◽  
...  
Keyword(s):  
Cholesterol Metabolism ◽  
Carrier Protein ◽  
Biliary Lipid ◽  
Sterol Carrier Protein ◽  
Hepatic Cholesterol ◽  
Sterol Carrier Protein 2

Abstract 65: Flavin Monoxygenase 3 (FMO3) is a Novel Regulator of Hepatic Cholesterol Metabolism and Transintestinal Cholesterol Efflux (TICE).

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Manya Warrier ◽  
Stepahie Marshall ◽  
Allison McDaniel ◽  
Martha Wilson ◽  
Amanda Brown ◽  
...  
Keyword(s):  
Cholesteryl Ester ◽  
Plasma Levels ◽  
Cholesterol Efflux ◽  
Cholesterol Metabolism ◽  
Transcriptional Profiling ◽  
Dietary Cholesterol ◽  
High Cholesterol Diet ◽  
Hepatic Cholesterol ◽  
Hepatic Expression ◽  
Cholesterol Levels

Recent studies have revealed a novel route for cholesterol disposal through intestine known as transintestinal cholesterol efflux (TICE) that significantly contributes to fecal neutral sterol loss. This pathway is an integral part of reverse cholesterol transport (RCT), yet major mechanisms regulating TICE are not well understood. Using an unbiased transcriptional profiling approach in mouse models of augmented TICE, we found that hepatic expression of the enzyme Flavin monoxygenase 3 (FMO3) was dramatically repressed. At the same time we identified this enzyme through transcriptional profiling, it was reported that plasma levels of its product trimethylamineoxide (TMAO) are highly predictive of atheroslcerosis in humans, and TMAO is proatherogenic in mice. To further understand FMO3’s role as a regulator of cholesterol metabolism we used antisense oligonucleotides (ASO) to knockdown FMO3 expression in mouse liver in C57BL/6 mice fed either low (0.02%) or high (0.2%) levels of dietary cholesterol. As expected, FMO3 knockdown (>90% knockdown in the liver) increased the TMA/TMAO ratio in plasma more than 3-fold. Interestingly, knockdown of FMO biliary cholesterol levels were reduced by 60%, whereas fecal cholesterol loss was quite normal in FMO3 ASO treated mice fed a high cholesterol diet, which phenocopies a previously described mouse model where TICE predominates (NPC1L1-liver transgenic mice). ASO-mediated knockdown of FMO3 also unexpectedly reduced hepatic cholesteryl ester (CE) storage by 70% in mice fed 0.2% cholesterol. In parallel, knockdown of FMO3 reduces plasma VLDL cholesterol levels and the secretion rate of VLDL cholesteryl ester, but not triacylglycerol in cholesterol fed mice. FMO3 knockdown also reduced the hepatic expression of several liver X receptor (LXR) target genes, while increasing expression of genes involved in cholesterol synthesis. Collectively, these studies have identified FMO3 as a novel regulator of hepatic cholesterol metabolism and TICE. Given that plasma levels of FMO3’s product (TMAO) are strongly associated with atherosclerosis development in humans, and production of TMAO promotes atherosclerosis in mice, these studies have important implications for future cardiovascular drug discovery.

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