Niacin therapy in atherosclerosis

Meyers, Charles D.; Kamanna, Vajinath S; Kashyap, Moti L.

doi:10.1097/00132980-200502000-00005

Cited by 127 publications

(52 citation statements)

References 45 publications

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“…HepG2 cells ( ‫ف‬ 70% confl uence) were incubated with niacin for ‫ف‬ 24-48 h and then labeled with 2uCi/ml 3 H-choline or 3 Hcholesterol in DMEM containing 5 mg/ml BSA free of fatty acids Niacin is the most potent currently available pharmacologic agent to increase HDL (10)(11)(12)(13). Interestingly, niacin selectively increases plasma HDL particles con taining mainly apoA-I (LP-AI, HDL subclasses with cardioprotective properties) but not HDL particles containing both apoA-I and A-II (LP-AI+AII) ( 15 ).…”

Section: Cholesterol and Phospholipid Effl Uxmentioning

confidence: 99%

Niacin increases HDL biogenesis by enhancing DR4-dependent transcription of ABCA1 and lipidation of apolipoprotein A-I in HepG2 cells

Zhang

Kamanna

Ganji

et al. 2012

Journal of Lipid Research

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Section: Cholesterol and Phospholipid Effl Uxmentioning

confidence: 99%

Niacin increases HDL biogenesis by enhancing DR4-dependent transcription of ABCA1 and lipidation of apolipoprotein A-I in HepG2 cells

Zhang

Kamanna

Ganji

et al. 2012

Journal of Lipid Research

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“…HDL has also been shown to have the other cardio-protective properties of antiinflammation, anti-oxidation, and anti-thrombosis (2). Niacin (nicotinic acid), a water-soluble vitamin and the most effective clinical agent in elevating plasma HDL-C and apolipoprotein A-I (apoA-I) levels, has been widely used in the treatment of dyslipidemia (3)(4)(5)(6)(7)(8). Either as monotherapy or in combination with other lipid-lowering agents, niacin significantly reduces cardiovascular risk.…”

mentioning

confidence: 99%

“…Furthermore, long-term follow-up of patients in the Coronary Drug Project with coronary arteriographic studies including the Cholesterol Lowering Atherosclerosis Studies, and the Familial Atherosclerosis Treatment Study, ARBITER 2 study, indicated that treatment with niacin significantly reduced total mortality and coronary events and retarded progression and even induced regression of coronary atherosclerosis (as reviewed in Refs. [3][4][5][6].…”

mentioning

confidence: 99%

“…Although niacin has been commonly used to increase plasma HDL levels, the mechanism(s) by which niacin exerts its action is not clearly understood (4)(5)(6)(7)(8)(9)(10). Earlier kinetics studies showed that the rise in plasma apoA-I (major protein of HDL) in patients treated with niacin was a result of decreased fractional catabolic rates rather than alteration in its synthetic rates (7,8).…”

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confidence: 99%

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Niacin inhibits surface expression of ATP synthase β chain in HepG2 cells: implications for raising HDL

Zhang

Kamanna²,

Zhang³

et al. 2008

Journal of Lipid Research

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Niacin is an effective agent for raising HDL, but its cellular target sites are largely unknown. We examined effects of niacin on the surface expression of ATP synthase b chain, a newly described HDL/apolipoprotein A-I (apoA-I) receptor for HDL endocytosis, in HepG2 cells. A significant amount of immunodetectable b chain was observed on the surface of HepG2 cells, which was competitively displaced by apoA-I. Niacin treatment reduced the surface expression of b chain in HepG2 cells by ?27%, and decreased 125 I-labeled HDL uptake up to ?35%. However, nicotinamide, a niacin metabolite that does not have clinical lipid effects, exhibited weaker inhibition on the b chain cell surface expression, and failed to show inhibitory action on 125 I-labeled HDL uptake. Furthermore, anti-b chain antibody significantly reduced 125 I-labeled HDL uptake and abolished the inhibitory effect of niacin. Niacin did not change b chain mRNA expression. These data suggest that niacin inhibits cell surface expression of the ATP synthase b chain, leading to reduced hepatic removal of HDL protein, thus implicating a potential cellular target for niacin action to raise HDL.-Zhang, L-H., V. S. Kamanna, M. C. Zhang, and M. L. Kashyap. Niacin inhibits surface expression of ATP synthase b chain in HepG2 cells: implications for raising HDL.

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“…Niacin (nicotinic acid) has been used for more than 30 years to treat plasma lipid disorders and to prevent atherosclerotic cardiovascular disease [1]. Niaspan prolonged release tablets contain the active ingredient nicotinic acid (also known as niacin), which is a member of the group of B vitamins.…”

Section: Introductionmentioning

confidence: 99%

Niacin: Does It affect 8-hydroxy-2-deoxyguanosine levels of the patients having low HDL cholesterol levels?

Harman¹,

Akçay²,

Buke³

et al. 2013

Med-Science

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Niacin therapy in atherosclerosis

Cited by 127 publications

References 45 publications

Niacin increases HDL biogenesis by enhancing DR4-dependent transcription of ABCA1 and lipidation of apolipoprotein A-I in HepG2 cells

Niacin increases HDL biogenesis by enhancing DR4-dependent transcription of ABCA1 and lipidation of apolipoprotein A-I in HepG2 cells

Niacin inhibits surface expression of ATP synthase β chain in HepG2 cells: implications for raising HDL

Niacin: Does It affect 8-hydroxy-2-deoxyguanosine levels of the patients having low HDL cholesterol levels?

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