Words similar to hmg-coa
Example sentences for: hmg-coa
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Statins, potent compounds that inhibit cholesterol synthesis in the liver by blocking 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA), have been reported to induce osteoblast activity and lead to bone formation, both in tissue culture and in rats and mice [ 1 2 3 4 5 6 ] . These findings, if confirmed and extended to include humans, have the potential to introduce immediate new treatment options to patients with low bone mass and osteoporosis.
Statins inhibit HMG-CoA reductase—a key enzyme in the cholesterol synthesis pathway.
The relative amounts of Abcg5 , Abcg8 , Cyp7a1, HMG-CoA reductase, and Srebp-2 message from rat liver samples used in real-time RT-PCR were normalised to GAPDH expression levels to compensate for variations in input RNA amounts.
It is generally accepted that the hydroxy acid form of statins are potent inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, an enzyme that plays a critical role in cholesterol metabolism, where they block substrate accessibility to HMG-CoA reductase, effectively subverting cholesterol levels of HDL [ 19 20 21 ] . In addition to lowering cholesterol, statins seem to have a number of additional effects, such as the nitric oxide-mediated promotion of new blood vessel growth [ 22 ] , protection against oxidative modification of low-density lipoprotein, as well as anti-inflammatory effects and a reduction in C-reactive protein levels [ 23 ] . All statins limit cholesterol biosynthesis by inhibiting the committed step in the biosynthesis of isoprenoids and sterols [ 24 ] .
These compounds can activate some nuclear receptors including steroidogenic factor 1 [ 44 ] and LXR, which may be partially responsible for their biological activities [ 45 46 ] . Cholesterol oxides are inhibitors of HMG-CoA reductase, the key enzyme of cholesterol biosynthesis pathway [ 47 ] . The ability to bind to an intracellular receptor, oxysterol binding protein, may be responsible for their inhibition of cholesterol biosynthesis [ 48 49 ] . It should be noted that addition of cholesterol does not prevent cholesterol oxide induced cell death, which leads to the suggestion that inhibition of cholesterol synthesis is not the cause of cholesterol oxide induced PCD [ 50 51 ] . The critical events that result in cholesterol oxide induced cytotoxicity remain to be determined.
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