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Mechanism of action of niacin.
TLDR
Initial data suggest that niacin, by inhibiting the hepatocyte surface expression of beta-chain adenosine triphosphate synthase (a recently reported HDL-apo A-I holoparticle receptor), inhibits the removal of HDL-AP-I. Expand
Dulaglutide and cardiovascular outcomes in type 2 diabetes (REWIND): a double-blind, randomised placebo-controlled trial
TLDR
Dulaglutide could be considered for the management of glycaemic control in middle-aged and older people with type 2 diabetes with either previous cardiovascular disease or cardiovascular risk factors. Expand
Niacin inhibits vascular oxidative stress, redox-sensitive genes, and monocyte adhesion to human aortic endothelial cells.
TLDR
Initial data presented herein support the novel concept that niacin has vascular anti-inflammatory and potentially anti-atherosclerotic properties independent of its effects on lipid regulation. Expand
Relation of gemfibrozil treatment and lipid levels with major coronary events: VA-HIT: a randomized controlled trial.
TLDR
Concentrations of HDL-C achieved with gemfibrozil treatment predicted a significant reduction in CHD events in patients with low LDL-C levels, however, the change in HDL- C levels only partially explained the beneficial effect of gem fibroZil. Expand
Comparative effects on lipid levels of combination therapy with a statin and extended-release niacin or ezetimibe versus a statin alone (the COMPELL study).
TLDR
Low to moderate dose combination therapy with a statin and niacin ER provided broad control of lipids and lipoproteins independently associated with CHD, and Statin/niacin ER combination regimens also increased HDL-C and large HDL (HDL2) and lowered triglycerides andlipoprotein significantly more than other regimens. Expand
Niacin and cholesterol: role in cardiovascular disease (review).
TLDR
Evidence is provided to extend the role of niacin as a lipid-lowering drug beyond its role as a vitamin. Expand
Long-term safety and efficacy of a once-daily niacin/lovastatin formulation for patients with dyslipidemia.
TLDR
Once-daily niacin/lovastatin exhibits substantial effects on multiple lipid risk factors and represents a significant new treatment option in the management of dyslipidemia. Expand
Niacin accelerates intracellular ApoB degradation by inhibiting triacylglycerol synthesis in human hepatoblastoma (HepG2) cells.
TLDR
Data indicate that niacin accelerates hepatic intracellular post-translational degradation of apoB by selectively reducing triglyceride synthesis (through inhibiting both fatty acid synthesis and fatty acid esterification to produce TG) without affecting ALLN-inhibitable protease- or MTP-mediated intrACEllular apoBs processing, resulting in decreased apo B secretion and hence lower circulating levels of the atherogenic lipoproteins. Expand
Interchange of apolipoproteins between chylomicrons and high density lipoproteins during alimentary lipemia in man.
TLDR
The results obtained demonstrate that high density lipoproteins contribute certain functionally important polar constituents to chylomicrons during alimentary lipemia in man and suggest that they also receive surface constituents from chylomaticrons during the course of their metabolism. Expand
Niacin inhibits surface expression of ATP synthase beta chain in HepG2 cells: implications for raising HDL.
TLDR
It is suggested that niacin inhibits cell surface expression of the ATP synthase beta chain, leading to reduced hepatic removal of HDL protein, thus implicating a potential cellular target for niacIn action to raise HDL. Expand
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