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Atorvastatin may protect the liver and blood vessels from diet-related fatty liver disease by restoring key bile acid signals
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Abstract
Mice fed a high fat/high cholesterol diet are protected from a harmful lipid profile due to enhanced cholesterol disposal through bile acids.
- Muricholic acids generated from chenodeoxycholic acid suppress FXR signaling in the liver, acting as antagonists.
- Treatment with obeticholic acid, an FXR agonist, did not improve liver histopathology in mice on a high fat diet.
- Obeticholic acid treatment reduced the expression of genes involved in bile acid synthesis and excretion.
- Atorvastatin treatment mitigated liver and vascular injury from a high fat diet and increased bile acid synthesis and excretion.
- Atorvastatin promoted the growth of bacteria that enhance the formation of beneficial bile acids in the intestine.
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