scholarly journals Rspo1/Rspo3‐LGR4 signaling inhibits hepatic cholesterol synthesis through the AMPKα‐SREBP2 pathway

2020 ◽  
Vol 34 (11) ◽  
pp. 14946-14959
Author(s):  
Shiying Liu ◽  
Yuan Gao ◽  
Liping Zhang ◽  
Yue Yin ◽  
Weizhen Zhang
Keyword(s):  
Cholesterol Synthesis ◽  
Hepatic Cholesterol ◽  
Hepatic Cholesterol Synthesis

Increased hepatic cholesterol synthesis in normal rats by cross-circulation with ileal bypassed partners

1979 ◽  
Vol 34 (4) ◽  
pp. 383-389 ◽  
Author(s):  
Philip D. Schneider ◽  
Ignacio J. Guzman ◽  
Richard D. Rucker ◽  
Thomas G. Stocks ◽  
Richard L. Varco ◽  
...  
Keyword(s):  
Cholesterol Synthesis ◽  
Hepatic Cholesterol ◽  
Hepatic Cholesterol Synthesis

Selective effects of two novel squalene synthase inhibitors on hepatic cholesterol synthesis in the rat

1994 ◽  
Vol 109 (1-2) ◽  
pp. 252 ◽  
Author(s):  
G.J. Smith ◽  
R.G. Davidson ◽  
C. Dunkley ◽  
G.R. Brown ◽  
K.B. Mallion ◽  
...  
Keyword(s):  
Cholesterol Synthesis ◽  
Squalene Synthase ◽  
Hepatic Cholesterol ◽  
Hepatic Cholesterol Synthesis ◽  
Selective Effects

High plasma cholesterol in drug-induced cholestasis is associated with enhanced hepatic cholesterol synthesis

1999 ◽  
Vol 276 (5) ◽  
pp. G1165-G1173 ◽  
Author(s):  
Jeffrey W. Chisholm ◽  
Patrick Nation ◽  
Peter J. Dolphin ◽  
Luis B. Agellon
Keyword(s):  
Bile Acids ◽  
Cholesterol Synthesis ◽  
Cell Membranes ◽  
Reductase Activity ◽  
Plasma Cholesterol ◽  
Hepatic Cell ◽  
Plasma Lipoproteins ◽  
Liver Cholesterol ◽  
Hepatic Cholesterol ◽  
Hepatic Cholesterol Synthesis

In α-naphthylisothiocyanate-treated mice, plasma phospholipid (PL) levels were elevated 10- and 13-fold at 48 and 168 h, respectively, whereas free cholesterol (FC) levels increased between 48 h (17-fold) and 168 h (39-fold). Nearly all of these lipids were localized to lipoprotein X-like particles in the low-density lipoprotein density range. The PL fatty acyl composition was indicative of biliary origin. Liver cholesterol and PL content were near normal at all time points. Hepatic hydroxymethylglutaryl CoA reductase activity was increased sixfold at 48 h, and cholesterol 7α-hydroxylase activity was decreased by ∼70% between 24 and 72 h. These findings suggest a metabolic basis for the appearance of abnormal plasma lipoproteins during cholestasis. Initially, PL and bile acids appear in plasma where they serve to promote the efflux of cholesterol from hepatic cell membranes. Hepatic cholesterol synthesis is then likely stimulated in the response to the depletion of hepatic cell membranes of cholesterol. We speculate that the enhanced synthesis of cholesterol and impaired conversion to bile acids, particularly during the early phase of drug response, contribute to the accumulation of FC in the plasma.

scholarly journals Effects of dietary polychlorinated biphenyls on cholesterol catabolism in rats

1990 ◽  
Vol 64 (1) ◽  
pp. 161-169 ◽  
Author(s):  
Satoshi Nagaoka ◽  
Hitoshi Miyazaki ◽  
Yoritaka Aoyama ◽  
Akira Yoshida
Keyword(s):  
Polychlorinated Biphenyls ◽  
Bile Acids ◽  
Cholesterol Synthesis ◽  
Control Group ◽  
Hepatic Cholesterol ◽  
Biliary Cholesterol ◽  
Faecal Excretion ◽  
Hepatic Cholesterol Synthesis ◽  
Total Bile Acids

Dietary polychlorinated biphenyls (PCBs) caused hypercholesterolaemia in rats. The concentration and output of biliary cholesterol was significantly lower than that of the control group. Biliary output of total bile acids was significantly decreased in rats given the PCB-supplemented diet. Faecal excretion of total steroids (sum of neutral steroids and acidic steroids) was not significantly changed in rats given the PCB-supplemented diet. The present results indicate that dietary PCBs cause hypercholesterolaemia without modifying the faecal total steroids excretion. These results suggest that PCBs produce hyper-cholesterolaemia accompanied by changes in biliary or faecal excretion of bile acids and neutral steroids in addition to an increase in hepatic cholesterol synthesis.

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