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Table of Contents
Disruption of CYP7A1 from classic bile acid synthesis in mice leads to either increased postnatal death or a milder phenotype with elevated serum cholesterol.  The latter is similar to the case in humans, where CYP7A1 mutations associate with high plasma low-density lipoprotein and hepatic cholesterol content, as well as deficient bile acid excretion. There is also a synergy between plasma low-density lipoprotein cholesterol (LDL-C) and risks of coronary artery disease (CAD).  Glucose signaling also induces CYP7A1 gene transcription by epigenetic regulation of the histone acetylation status. Glucose induction of bile acid synthesis have an important implication in metabolic control of glucose, lipid, and energy homeostasis under normal and diabetic conditions.  CYP7A1-rs3808607 and APOE isoform are associated with the extent of reduction in circulating LDL cholesterol in response to PS ( define PS, Plant Sterol? ) consumption and could serve as potential predictive genetic markers to identify individuals who would derive maximum LDL cholesterol lowering with PS consumption.  Genetic variations in CYP7A1 influence its expression and thus may affect the risk of gallstone disease and Galbaldder Cancer.