Sentences with phrase «coa reductase»

A key enzyme in cholesterol biosynthesis is 3 - hydroxy -3-methylglutaryl — CoA reductase (the target for statins), which is activated by insulin, which means that an increase in blood glucose and consequently of insulin levels will lead to increased endogenous cholesterol synthesis.
In animal studies, propionic acid has been shown to inhibit HMG - CoA reductase, an enzyme involved in the production of cholesterol by the liver.
Statins such as Lipitor, Zocor, Pavacol and Mevacor lower cholesterol by inhibiting HMG - CoA reductase, a key enzyme in cholesterol synthesis.
Statin drugs like Lipitor, Crestor and Lovastatin are called HMG - CoA reductase inhibitors.
They also inhibit the cholesterol - producing enzyme HMG - CoA reductase in the liver, which lowers LDL, and in other cells (including the brain) which can produce both benefits and harms (for example, this enzyme is also needed to make vitamin K2, which is important for sulfatide synthesis in the brain and hence cognition).
The FDA is now requiring drug companies to add an additional WARNING to their cholesterol lowering statins (or HMG - CoA reductase inhibitors).
Modern cholesterol - lowering drugs act by inhibiting an enzyme (HMG - CoA reductase) needed for the formation of cholesterol in the liver.
These HMG - CoA reductase inhibitors, called statins, are sold as Lipitor, Mevacor, Pravacol, Zocor, etc..
They fall under the drug category known as «HMG - CoA reductase inhibitors», meaning that they block the action of this enzyme in the body.
The HMG - CoA reductase enzyme is responsible for making cholesterol.
Modern research reveals that red yeast rice contains number of compounds that act as natural HMG - CoA reductase inhibitors, similar to the cholesterol - lowering ingredient found in pharmaceutical statin drugs.
Inhibition of HMG - CoA reductase also blocks production of Co-Enzyme Q10.
Statins are HMG - CoA reductase inhibitors, that is, they act by blocking the enzyme in your liver that is responsible for making cholesterol (HMG - CoA reductase).
Vitamin K2 MK4 formation in brain is HMG - CoA reductase dependent; MK4 prevents congnitive decline by catalysing myelin sulfatide synthesis.
Albert, A. W. Lovastatin and simvastatin - inhibitors of HMG CoA reductase and cholesterol - biosynthesis.
In fact, high cholesterol levels later in life are associated with reduced risk of dementia, and the CSF of AD patients has been shown to be lower in cholesterol than that of healthy controls.62, 63 HMG CoA reductase — the target of statin therapy — is abundant in brain cells.
Eight controlled clinical trials have shown that statin drugs cause Coenzyme Q10 depletion by inhibition of HMG - CoA reductase, which is the rate limiting step in cholesterol and Coenzyme Q - 10 biosynthesis.
Competitive Inhibitors of HMG - CoA Reductase, aka «Statins» «Statins» block a key step in the formation of cholesterol.
This complex synthesis involves 37 steps and starts with a key enzyme known as HMG - CoA reductase (inhibited by statins, a class of cholesterol - lowering drugs).
These medications are able to block the action of an enzyme called HMG CoA reductase (7,11) that is necessary for making cholesterol in the liver.
Abstract: Background: Treatment with HMG - CoA reductase inhibitors («statins») has been variably associated with a reduced risk of Alzheimer's disease (AD) in epidemiologic studies and reduced amyloid - β (Aβ) deposition in animal models of AD.
Background: Treatment with HMG - CoA reductase inhibitors («statins») has been variably associated with a reduced risk of Alzheimer's disease (AD) in epidemiologic studies and reduced amyloid - β (Aβ) deposition in animal models of AD.
Statins inhibit the enzyme HMG - CoA reductase, one of the MVP's key components.
But other lipids are known to guide cell migrations in human brain development, and geneticist Ken Howard of University College London suspects HMG - CoA reductase might help produce a similar lipid molecule or modify a protein that attracts the germ cells.
The guideline identifies four major groups of patients for whom cholesterol - lowering HMG - CoA reductase inhibitors, or statins, have the greatest chance of preventing stroke and heart attacks.
Isoprenoid - mediated suppression of HMG CoA reductase in tumors was previously correlated to growth arrest; the latter was attenuated by supplemental mevalonate.
They further show that this diterpine downregulates HMG CoA reductase offering support to the concept that mevalonate deprivation causes cell cycle arrest at the G1 phase leading to apoptotic death of the prostate carcinoma cells.
In collaboration with the University of Texas Southwestern Medical Center (UTSW) in Dallas, the researchers found that the tumor - suppressive activity of geranylgeraniol was accompanied by down - regulation of HMG CoA reductase, a key enzyme in the mevalonate pathway that provides essential intermediates for the posttranslational modification of growth - related proteins such as Ras, nuclear lamins and insulin - like growth factor receptors.
Statins block the action of an enzyme, HMG - CoA reductase, which is essential to the process.
Returning to Japan, he happened upon a compound in a fermented broth of Penicillium citrinum, a rice mold taken from a shop in Kyoto, that blocked the action of HMG - CoA reductase.

Not exact matches

More than 30 different enzymes orchestrate the process, but one central to the assembly line is called 3 - hydroxy -3-methylglutaryl-CoA (or HMG - CoA) reductase, an early step in a long line of steps.
HMG - CoA (3 - hydroxy -3-methylglutaryl — coenzyme A) reductase (HMGR) catalyzes the committed step in cholesterol biosynthesis.
Possible Interactions Certain medications such as Adriamycin, lovastatin and other HMG CoA - reductase inhibitors, gemfibrozil, beta - blockers, tricyclic antidepressants, and phenothiazine may deplete the body of coenzyme Q10.
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