Disease relevance of Schol

• In liver-Cpr-null (with liver-specific Cpr deletion) and Cpr-low (with reduced CPR expression in all organs examined) mouse models, a reduced serum cholesterol level and an induction of hepatic P450s were observed, whereas hepatomegaly and fatty liver were only observed in the liver-Cpr-null model [1].
• After 10 d, a dose of 1000 mg eicosapentaenoic acid per day/kg body weight lowered serum triglycerides by 45%, while no significant change in serum cholesterol level was noted in comparison to palmitic acid fed mice and controls [2].
• In the control group, the serum cholesterol level increased due to the development of glomerulonephritis [3].

High impact information on Schol

• Therefore, some aspects like loss of body fat are better studied in mice; for other aspects like reduction in serum cholesterol level the rat may be the model of choice [4].
• LDLR(-/-) and ApoE(-/-) mice fed the normal diet showed significantly higher serum cholesterol level than that of C57BL/6 mice fed the high-fat diet [5].
• The most potent compound, SM-32504 (3m), decreased the serum cholesterol level significantly in a high fat and high cholesterol-fed mouse model [6].
• Feeding a high fat diet supplemented with fenofibrate (0.05% w/w) reduced all of these effects significantly in males except serum cholesterol level [7].
• It was found that orally administered (-)-epicatechin gallate and (-)-epigallocatechin gallate from tea leaves lowered the serum cholesterol level in mice fed a high fat emulsion [8].

Anatomical context of Schol

• Oral administration of Shosaikoto significantly suppressed the elevation of serum cholesterol in C57BL/6 mice fed a 1.25% cholesterol-enriched diet for four weeks and improved the T cell ratio in peripheral blood, which decreased with the increase of the serum cholesterol level [9].

Associations of Schol with chemical compounds

• 1) In Triton-induced hyperlipemic mice, AAS (300 mg/kg) significantly decreased the serum cholesterol level, while L-ascorbate (AA, 175 mg/kg) was found ineffective [10].

Analytical, diagnostic and therapeutic context of Schol

• On a severe atherogenic diet, the homozygous apoC1-deficient mice become hypercholesterolaemic, with a serum cholesterol level of 10.7 +/- 3.3 mM compared with 6.7 +/- 1.8 mM and 5.1 +/- 1.6 mM in heterozygous and control mice respectively [11].

References