Disease relevance of Lcho1

• No differences were found between mice, with or without gallstones, in plasma and liver cholesterol levels, biliary phospholipid and bile acid levels, fecal sterol and bile acid levels, and biliary and fecal bile acid composition [1].

High impact information on Lcho1

• Transgene expression only modestly affected plasma and liver cholesterol levels but profoundly altered cholesterol transport [2].
• RESULTS: ALT, plasma homocysteine, liver cholesterol, and TUNEL positive hepatocytes were increased in alcohol-fed mice as compared to control in both genotypes [3].
• ApoE knockout mice were infected with T. gondii, and at 5 weeks of infection, serum, feces, and liver cholesterol; aortic lesion size, cellularity, and inflammatory cytokines; and levels of serum nitrite and gamma interferon (IFN-gamma) were analyzed [4].
• Melatonin treatment was found to reduce plasma, liver cholesterol and DC levels as well as liver triglyceride levels in hypercholesterolemic mice [5].
• In wild-type C57BL/6 mice, feeding increasing amounts of HDCA resulted in i) progressive decrease in dietary cholesterol absorption, ii) increased concentrations of HDCA in the gallbladder bile, iii) decreased liver cholesterol content, iv) increased liver cholesterol synthesis, and v) increased plasma concentrations of HDCA [6].

Chemical compound and disease context of Lcho1

• Feeding a high cholesterol, high cholic acid diet to mice for 28 days caused increased concentrations of plasma and liver cholesterol and formation of gallstones [7].

Biological context of Lcho1

• The results showed that the Chol + SFA diet decreased CYP7alpha1 gene expression and bile acid pool size, resulting in increased blood and liver cholesterol levels [8].

Anatomical context of Lcho1

• Plasma and liver cholesterol were measured; pancreata, intestinal contents and mucosal scrapes were collected for bile acid, trypsin, chymotrypsin, amylase, and lipase assays [9].
• Tissue lipids were reduced by these agents e.g. liver cholesterol, and triglyceride and small intestine mucosa cholesterol levels [10].

Associations of Lcho1 with chemical compounds

• Cholesterol- and bile acid-controlled liver cholesterol 7alpha-hydroxylase, the limiting enzyme for bile acid synthesis, was elevated, unresponsive to dietary cholesterol, but repressed normally by dietary cholate [11].
• In 56 day old npc1(-/-) mice that had been fed from 35 days of age a rodent diet or the same diet containing either cholesterol (1.0%, w/w) or ezetimibe (a sterol absorption inhibitor; 0.0125%, w/w), whole liver cholesterol content averaged 33.5 +/- 1.1, 87.9 +/- 1.7, and 20.8 +/- 0.9 mg, respectively [12].
• As previously reported by us, mice with targeted disruption of the CYP8B1 gene (CYP8B1-/-) fail to produce cholic acid (CA), upregulate their bile acid synthesis, reduce the absorption of dietary cholesterol and, after cholesterol feeding, accumulate less liver cholesterol than wild-type (CYP8B1+/+) mice [13].
• Plasma and liver cholesterol levels were decreased by ursodeoxycholic acid but not by ursocholic acid [1].
• Effects of spinasterol and sitosterol on plasma and liver cholesterol levels and biliary and fecal sterol and bile acid excretions in mice [14].

Other interactions of Lcho1

• Dietary isohumulones, the bitter components of beer, raise plasma HDL-cholesterol levels and reduce liver cholesterol and triacylglycerol contents similar to PPARalpha activations in C57BL/6 mice [15].
• Addition of cholesterol to the diets (1%, w/w) greatly increased liver cholesterol levels but did not affect the corn oil effect upon liver and plasma cholesterol [16].
• The increase in plasma and liver cholesterol levels after the feeding of the lithogenic diet was prevented by ileectomy [17].

Analytical, diagnostic and therapeutic context of Lcho1

• A 28-day immobilization stress schedule was used to induce increases in plasma, aortic and liver cholesterol of mice maintained on a high cholesterol diet [18].
• Taurine significantly increased CYP7A1 mRNA levels in the CBT-group compared with the CB-group in both animal models, with a subsequent decrease in serum and liver cholesterol levels and increase in fecal bile acid excretion [19].
• The hepatic cholesterol concentration in all the seafood groups was significantly lower than that in the control group, and defatting did not influence the liver cholesterol concentration [20].

References