How a cholesterol drug cuts bad cholesterol in pigs
Inhibition of HMG-CoA reductase by atorvastatin decreases both VLDL and LDL apolipoprotein B production in miniature pigs.
Not medical advice. For informational purposes only. Always consult a healthcare professional. Terms
Surprising Findings
Atorvastatin reduced hepatic apoB mRNA by 13% but left LDL receptor mRNA unchanged.
It’s widely believed statins lower LDL by increasing LDL receptor expression; this study shows no such effect, suggesting a novel mechanism.
Practical Takeaways
Don’t assume animal studies directly translate to human statin effects.
Not medical advice. For informational purposes only. Always consult a healthcare professional. Terms
Surprising Findings
Atorvastatin reduced hepatic apoB mRNA by 13% but left LDL receptor mRNA unchanged.
It’s widely believed statins lower LDL by increasing LDL receptor expression; this study shows no such effect, suggesting a novel mechanism.
Practical Takeaways
Don’t assume animal studies directly translate to human statin effects.
Publication
Journal
Arteriosclerosis, thrombosis, and vascular biology
Year
1997
Authors
John R. Burnett, L. Wilcox, D. E. Telford, S. Kleinstiver, P. Barrett, Roger S. Newton, M. W. Huff
Related Content
Claims (6)
Inhibition of hepatic HMG-CoA reductase reduces circulating LDL cholesterol by decreasing endogenous cholesterol synthesis and upregulating hepatic LDL receptor expression.
The drug seemed to make less of the bad cholesterol particle by turning fewer big particles into smaller ones, but this effect wasn’t strong enough to be sure it wasn’t just chance.
The drug lowered the genetic instructions in the liver for making the bad cholesterol protein, but didn’t change the instructions for clearing it from the blood.
The drug lowered several types of bad fats in the pigs’ blood — including total cholesterol, LDL cholesterol, and triglycerides — by up to 31%.
Giving pigs a cholesterol-lowering drug called atorvastatin for three weeks made their livers produce less of a key protein (apoB) that helps form bad cholesterol particles, without changing how fast those particles were cleared from the blood.