[300] HEPATIC EXPRESSION OF NUCLEAR RECEPTORS AND BILIARY TRANSPORTERS IN HUMAN CHOLESTEROL GALLSTONE DISEASE

2007 ◽  
Vol 46 ◽  
pp. S119 ◽  
Author(s):  
M. Bertolotti ◽  
C. Gabbi ◽  
C. Anzivino ◽  
E. Tagliafico ◽  
L. Carulli ◽  
...  
2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Mary Carmen Vázquez ◽  
Attilio Rigotti ◽  
Silvana Zanlungo

Cholesterol gallstone disease is highly prevalent in western countries, particularly in women and some specific ethnic groups. The formation of water-insoluble cholesterol crystals is due to a misbalance between the three major lipids present in the bile: cholesterol, bile salts, and phospholipids. Many proteins implicated in biliary lipid secretion in the liver are regulated by several transcription factors, including nuclear receptors LXR and FXR. Human and murine genetic, physiological, pathophysiological, and pharmacological evidence is consistent with the relevance of these nuclear receptors in gallstone formation. In addition, there is emerging data that also suggests a role for estrogen receptor ESR1 in abnormal cholesterol metabolism leading to gallstone disease. A better comprehension of the role of nuclear receptor function in gallstone formation may help to design new and more effective therapeutic strategies for this highly prevalent disease condition.


2022 ◽  
Vol 13 (1) ◽  
Author(s):  
Hai Hu ◽  
Wentao Shao ◽  
Qian Liu ◽  
Ning Liu ◽  
Qihan Wang ◽  
...  

AbstractCholesterol gallstone disease is a worldwide common disease. Cholesterol supersaturation in gallbladder bile is the prerequisite for its pathogenesis, while the mechanism is not completely understood. In this study, we find enrichment of gut microbiota (especially Desulfovibrionales) in patients with gallstone disease. Fecal transplantation of gut microbiota from gallstone patients to gallstone-resistant strain of mice can induce gallstone formation. Carrying Desulfovibrionales is associated with enhanced cecal secondary bile acids production and increase of bile acid hydrophobicity facilitating intestinal cholesterol absorption. Meanwhile, the metabolic product of Desulfovibrionales, H2S increase and is shown to induce hepatic FXR and inhibit CYP7A1 expression. Mice carrying Desulfovibrionales present induction of hepatic expression of cholesterol transporters Abcg5/g8 to promote biliary secretion of cholesterol as well. Our study demonstrates the role of gut microbiota, Desulfovibrionales, as an environmental regulator contributing to gallstone formation through its influence on bile acid and cholesterol metabolism.


1991 ◽  
Vol 32 (3) ◽  
pp. 469-475
Author(s):  
E Reihnér ◽  
B Angelin ◽  
I Björkhem ◽  
K Einarsson

2000 ◽  
Vol 118 (5) ◽  
pp. 912-920 ◽  
Author(s):  
Stefano Ginanni Corradini ◽  
Walter Elisei ◽  
Luca Giovannelli ◽  
Cristina Ripani ◽  
Paola Della Guardia ◽  
...  

2000 ◽  
Vol 4 (1) ◽  
pp. 59-65 ◽  
Author(s):  
BEVERLY PAIGEN ◽  
NICHOLAS J. SCHORK ◽  
KAREN L. SVENSON ◽  
YIN-CHAI CHEAH ◽  
JIAN-LONG MU ◽  
...  

Quantitative trait locus (QTL) mapping was used to locate genes that determine the difference in cholesterol gallstone disease between the gallstone-susceptible strain C57L/J and the gallstone-resistant strain AKR/J. Gallstone weight was determined in 231 male (AKR × C57L) F1× AKR backcross mice fed a lithogenic diet containing 1% cholesterol, 0.5% cholic acid, and 15% butterfat for 8 wk. Mice having no stones and mice having the largest stones were genotyped at ∼20-cM intervals to find the loci determining cholesterol gallstone formation. The major locus, Lith1, mapped near D2Mit56 and was confirmed by constructing a congenic strain, AK.L- Lith1s. Another locus, Lith2, mapped near D19Mit58 and was also confirmed by constructing a congenic strain AK.L- Lith2s. Other suggestive, but not statistically significant, loci mapped to chromosomes 6, 7, 8, 10, and X. The identification of these Lith genes will elucidate the pathophysiology of cholesterol gallstone formation.


2019 ◽  
Vol 26 (19) ◽  
pp. 3620-3638 ◽  
Author(s):  
Agostino Di Ciaula ◽  
Gabriella Garruti ◽  
Gema Frühbeck ◽  
Maria De Angelis ◽  
Ornella de Bari ◽  
...  

: Cholesterol gallstone disease is a major health problem in Westernized countries and depends on a complex interplay between genetic factors, lifestyle and diet, acting on specific pathogenic mechanisms. Overweigh, obesity, dyslipidemia, insulin resistance and altered cholesterol homeostasis have been linked to increased gallstone occurrence, and several studies point to a number of specific nutrients as risk- or protective factors with respect to gallstone formation in humans. There is a rising interest in the identification of common and modifiable dietetic factors that put the patients at risk of gallstones or that are able to prevent gallstone formation and growth. In particular, dietary models characterized by increased energy intake with highly refined sugars and sweet foods, high fructose intake, low fiber contents, high fat, consumption of fast food and low vitamin C intake increase the risk of gallstone formation. On the other hand, high intake of monounsaturated fats and fiber, olive oil and fish (ω-3 fatty acids) consumption, vegetable protein intake, fruit, coffee, moderate alcohol consumption and vitamin C supplementation exert a protective role. : The effect of some confounding factors (e.g., physical activity) cannot be ruled out, but general recommendations about the multiple beneficial effects of diet on cholesterol gallstones must be kept in mind, in particular in groups at high risk of gallstone formation.


2014 ◽  
Vol 20 (28) ◽  
pp. 9513-9518 ◽  
Author(s):  
Guo-Qiang Xu ◽  
Cheng-Fu Xu ◽  
Hong-Tan Chen ◽  
Shan Liu ◽  
Xiao-Dong Teng ◽  
...  

2018 ◽  
Vol 34 (2) ◽  
pp. 71-80 ◽  
Author(s):  
Agostino Di Ciaula ◽  
David Q.-H. Wang ◽  
Piero Portincasa

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