scholarly journals Biliary cholesterol excretion: A novel mechanism that regulates dietary cholesterol absorption

1998 ◽  
Vol 95 (17) ◽  
pp. 10194-10199 ◽  
Author(s):  
E. Sehayek ◽  
J. G. Ono ◽  
S. Shefer ◽  
L. B. Nguyen ◽  
N. Wang ◽  
...  
Keyword(s):  
Dietary Cholesterol ◽  
Cholesterol Absorption ◽  
Biliary Cholesterol ◽  
Cholesterol Excretion

Influence of dietary cholesterol on excretion of cholesterol-4-C14 by the rat

1962 ◽  
Vol 202 (6) ◽  
pp. 1073-1076 ◽  
Author(s):  
Jean D. Wilson
Keyword(s):  
Fatty Acids ◽  
Linoleic Acid ◽  
Bile Acid ◽  
Degradation Rate ◽  
Dietary Cholesterol ◽  
Cholesterol Absorption ◽  
Sterol Fraction ◽  
Acid Fraction ◽  
Neutral Sterol ◽  
Cholesterol Excretion

The influence of dietry cholesterol on the excretion of cholesterol-4-C14 has been studied in rats pair fed isocaloric quantities of purified diets supplemented with varying amounts of cholesterol and either oleic or linoleic acid. Of the C14 excreted over an 8-day period, slightly more than half was present in the neutral sterol fraction of feces from rats fed sterol-free diets. The addition of dietary cholesterol, however, under circumstances where significant cholesterol absorption was promoted by the addition of fatty acids to the diets, resulted in a reversal of this ratio so that the bile acid fraction accounted for the major portion of excreted cholesterol-C14. Cholesterol balance data revealed that the degradation rate of cholesterol in these animals rose to about 17–20 mg/day. These data are interpreted as demonstrating that the amount of absorbed dietary cholesterol plays a crucial role in determining both the relative and absolute importance of the two major routes of cholesterol excretion.

Abstract 621: Reduced Dietary Cholesterol Availability in Infancy Programs Cholesterol Absorption in Adult Mice

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Lidiya G Dimova ◽  
Jan F de Boer ◽  
Henkjan J Verkade ◽  
Uwe J Tietge
Keyword(s):  
Breast Milk ◽  
Cholesterol Metabolism ◽  
Dietary Cholesterol ◽  
Adult Life ◽  
Cholesterol Absorption ◽  
Suckling Period ◽  
Cholesterol Excretion ◽  
The Impact ◽  
Fecal Cholesterol ◽  
Endogenous Synthesis

Epidemiological research showed that feeding breast milk, which is rich in cholesterol, translates into reduced cardiovascular risk in adulthood compared to feeding formula, which is cholesterol free. The mechanisms underlying these observations are unclear. Therefore, the present study aimed to investigate the impact of reduced dietary cholesterol availability during the suckling period on cholesterol metabolism in adult life in mice. To achieve reduced dietary cholesterol exposure from breast milk LDLR knockout offspring were given the cholesterol absorption inhibitor ezetimibe for 3 weeks during the suckling period. Ezetimibe was added to the food of nursing dams and reached the offspring’s intestine via excretion into breast milk. Low cholesterol exposure (LC) mice were compared to normal cholesterol (NC) controls with respect to all relevant parameters of cholesterol metabolism including biliary and fecal cholesterol excretion, intestinal absorption and endogenous synthesis using stable isotope kinetics. At 24 weeks intestinal cholesterol absorption was decreased in LC mice (-30%, p<0.001) due to decreased Npc1l1 expression, the main intestinal cholesterol uptake transporter (-50%, p<0.05). Methylation analysis of the NPC1L1 promoter revealed substantial differences between jejunum and colon (p<0.001), but not between LC and NC. Plasma cholesterol levels were not different between NC and LC due to increased endogenous synthesis in the LC group (p<0.05). Food intake, biliary and fecal cholesterol excretion did not differ between groups. In summary, our results demonstrate that early life reduction of dietary cholesterol exposure programs the murine intestine in adulthood towards decreased cholesterol absorption via reduced Npc1l1 expression. These results support a key role of the intestine as sensor and integrator of cholesterol metabolism with high relevance for cardio-metabolic disease.

scholarly journals Biodynamics of cholesterol and bile acids in the lithiasic hamster

1991 ◽  
Vol 66 (3) ◽  
pp. 479-492 ◽  
Author(s):  
J. Khallou ◽  
M. Riottot ◽  
M. Parquet ◽  
C. Verneau ◽  
C. Lutton
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Cholesterol Synthesis ◽  
Specific Activity ◽  
Plasma Cholesterol ◽  
Dietary Cholesterol ◽  
Young Male ◽  
Cholesterol Absorption ◽  
Biliary Cholesterol ◽  
Faecal Excretion

By using the isotopic equilibrium method in the young male Syrian hamster, the rates of cholesterol turnover processes, i.e. dietary cholesterol absorption, cholesterol synthesis, cholesterol excretion in the faeces and urine and cholesterol transformation into bile acids, were determined in the hamster receiving a control (C) or a lithogenic diet (L) for 7 weeks. At the end of this period the gall bladder of all animals in group L contained cholesterol gallstones. The coefficient of dietary cholesterol absorption was reduced by 26 %, cholesterol synthesis and cholesterol faecal excretion were twofold higher in group L than in group C. Bile acid content in the small intestine was diminished in group L, but bile acid composition was similar in the two groups. The increase in cholesterogenesis in lithiasic animals essentially took place in the liver. Bile acid biosynthesis did not significantly differ in the two groups, but represented only 35 % of total cholesterol input (dietary absorption + internal secretion) in group L ν. 52% in group C. Thus, in the lithiasic hamster, hepatic synthesis of cholesterol and bile acids are not coupled. The molar percentage of cholesterol in bile was twofold higher in group L than in group C but those of bile acids and of phospholipids were not modified. In the lithiasic hamster the specific activity of biliary cholesterol was similar to that in plasma and liver. Consequently, biliary cholesterol does not derive directly from cholesterol newly synthesized in the liver but from hepatic cholesterol rapidly exchangeable with plasma cholesterol.

Progress in the Mechanism of Dietary Cholesterol Absorption

2012 ◽  
Vol 28 (7) ◽  
pp. 573
Author(s):  
Yingyu ZHANG ◽  
Baoliang SONG
Keyword(s):  
Dietary Cholesterol ◽  
Cholesterol Absorption

scholarly journals Dietary cholesterol absorption, and sterol and bile acid excretion in hypercholesterolemia-resistant white rabbits.

1990 ◽  
Vol 31 (11) ◽  
pp. 2019-2027
Author(s):  
ML Overturf ◽  
SA Smith ◽  
AM Gotto ◽  
JD Morrisett ◽  
T Tewson ◽  
...  
Keyword(s):  
Bile Acid ◽  
Dietary Cholesterol ◽  
Cholesterol Absorption ◽  
Acid Excretion ◽  
Bile Acid Excretion

scholarly journals A role for NPC1 and NPC2 in intestinal cholesterol absorption – the hypothesis gutted

2007 ◽  
Vol 408 (1) ◽  
Author(s):  
Laura Liscum
Keyword(s):  
Endoplasmic Reticulum ◽  
Dietary Cholesterol ◽  
Cholesterol Absorption ◽  
Cholesterol Transport ◽  
Intestinal Epithelial ◽  
Intestinal Cholesterol Absorption ◽  
Biochemical Journal ◽  
Good Target ◽  
Type C ◽  
Niemann Pick

Dietary and biliary cholesterol are taken up by intestinal epithelial cells and transported to the endoplasmic reticulum. At the endoplasmic reticulum, cholesterol is esterified, packaged into chylomicrons and secreted into the lymph for delivery to the bloodstream. NPC1L1 (Niemann–Pick C1-like 1) is a protein on the enterocyte brush-border membrane that facilitates cholesterol absorption. Cholesterol's itinerary as it moves to the endoplasmic reticulum is unknown, as is the identity of any cellular proteins that facilitate the movement. Two proteins that play an important role in intracellular cholesterol transport and could potentially influence NPC1L1-mediated cholesterol uptake are NPC1 and NPC2 (Niemann–Pick type C disease proteins 1 and 2). In this issue of the Biochemical Journal, Dixit and colleagues show that the absence or presence of NPC1 and NPC2 has no effect on intestinal cholesterol absorption in the mouse. Thus neither protein fills the gap in our knowledge of intra-enterocyte cholesterol transport. Furthermore, the NPC1/NPC2 pathway would not be a good target for limiting the uptake of dietary cholesterol.

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