Age- and Dietary Fat-Related Effects on Biliary Lipids and Cholesterol Gallstone Formation in African Green Monkeys

1992 ◽  
Vol 122 (4) ◽  
pp. 917-923 ◽  
Author(s):  
Martin W. Scobey ◽  
Mary S. Wolfe ◽  
Lawrence L. Rudel
2017 ◽  
Vol 312 (3) ◽  
pp. G266-G273 ◽  
Author(s):  
Devina Mehta ◽  
Kamal D. Mehta

Cholesterol homeostasis relies on an intricate network of cellular processes whose deregulation in response to Western type high-fat/cholesterol diets can lead to several life-threatening pathologies. Significant advances have been made in resolving the molecular identity and regulatory function of transcription factors sensitive to fat, cholesterol, or bile acids, but whether body senses the presence of both fat and cholesterol simultaneously is not known. Assessing the impact of a high-fat/cholesterol load, rather than an individual component alone, on cholesterol homeostasis is more physiologically relevant because Western diets deliver both fat and cholesterol at the same time. Moreover, dietary fat and dietary cholesterol are reported to act synergistically to impair liver cholesterol homeostasis. A key insight into the role of protein kinase C-β (PKCβ) in hepatic adaptation to high-fat/cholesterol diets was gained recently through the use of knockout mice. The emerging evidence indicates that PKCβ is an important regulator of cholesterol homeostasis that ensures normal adaptation to high-fat/cholesterol intake. Consistent with this function, high-fat/cholesterol diets induce PKCβ expression and signaling in the intestine and liver, while systemic PKCβ deficiency promotes accumulation of cholesterol in the liver and bile. PKCβ disruption results in profound dysregulation of hepatic cholesterol and bile homeostasis and imparts sensitivity to cholesterol gallstone formation. The available results support involvement of a two-pronged mechanism by which intestine and liver PKCβ signaling converge on liver ERK1/2 to dictate diet-induced cholesterol and bile acid homeostasis. Collectively, PKCβ is an integrator of dietary fat/cholesterol signal and mediates changes to cholesterol homeostasis.


1987 ◽  
Vol 32 (6) ◽  
pp. 609-614 ◽  
Author(s):  
Joel J. Roslyn ◽  
Robert L. Conter ◽  
Lawrence DenBesten

1988 ◽  
Vol 44 (6) ◽  
pp. 672-679 ◽  
Author(s):  
M.Samy Abdou ◽  
Seth D. Strichartz ◽  
Mohammad Z. Abedin ◽  
Joel J. Roslyn

Hepatology ◽  
1993 ◽  
Vol 18 (6) ◽  
pp. 1498-1503 ◽  
Author(s):  
Wayne W. Lamorte ◽  
Daniel P. O'Leary ◽  
Michael L. Booker ◽  
Thayer E. Scott

1975 ◽  
pp. 135-194 ◽  
Author(s):  
OSCAR W. PORTMAN ◽  
TOSHIAKI OSUGA ◽  
NAOMI TANAKA

1998 ◽  
Vol 79 (5) ◽  
pp. 463-471 ◽  
Author(s):  
Elke A. Trautwein ◽  
Angelika Kunath-Rau ◽  
Helmut F. Erbersdobler

The effect of high- (hePE) and low- (lePE) esterification pectin and high- (hvGG) and low-(lvGG) viscosity guar gum on plasma, hepatic and biliary lipids and on prevention of cholesterol gallstones was investigated in male golden Syrian hamsters (Mesocricetus auratus). Hamsters were fed on cholesterol-rich (4g/kg), gallstone-inducing diets for 6 weeks. The diets were supplemented with 80g hePE, lePE, hvGG or lvGG/kg or 80g additional cellulose/kg. No significant differences in plasma total cholesterol and triacylglycerol concentrations between hvGG and lvGG and the gallstone-inducing or cellulose-enriched diets were observed. The hePE diet produced a 16% (non-significant) reduction in total plasma cholesterol but significantly decreased the plasma triacylglycerol level by 45%. The lePE diet caused only minor changes in plasma lipids. Hepatic cholesterol concentrations were significantly higher in hamsters fed on hvGG, lvGG, hePE or lePE primarily due to the accumulation of esterified cholesterol. Supersaturated bile samples, with lithogenic indices ranging from 1.6 to 2.0, were determined with all diets. The hePE and lePE diets slightly altered the bile acid profile by increasing glycocholic acid and decreasing taurochenodeoxycholic acid concentrations resulting in a higher cholic: chenodeoxycholic acid ratio. Cholesterol gallstone formation was not substantially inhibited by the two varieties of pectin and guar gum. The hvGG, lvGG, hePE and lePE diets did not alter faecal weight and caused only minor increases in faecal bile acid excretion. In general, the present findings demonstrate that dietary pectins and guar gums had only minor effects on cholesterol metabolism and did not prevent cholesterol gallstone formation in this hamster model. Possible explanations for this lack of a distinct response to pectin and guar gum are discussed.


1998 ◽  
Vol 10 (12) ◽  
pp. A8
Author(s):  
K. J. van Erpecum ◽  
P. Portincasa ◽  
E. R.M. Eckhardt ◽  
B. J.M. van de Heijning ◽  
A. K. Groen ◽  
...  

2007 ◽  
Vol 133 (4) ◽  
pp. 1304-1315 ◽  
Author(s):  
Kirk J. Maurer ◽  
Varada P. Rao ◽  
Zhongming Ge ◽  
Arlin B. Rogers ◽  
Trisha J. Oura ◽  
...  

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