Niacin therapy in atherosclerosis

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

doi:10.1097/00041433-200412000-00006

Cited by 158 publications

(49 citation statements)

References 45 publications

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“…Niacin is efficacious at optimizing TG levels and HDL levels [95]. Niacin improves these lipid parameters through two mechanisms: (1) it increases sequestration of TGs in adipose (resulting in a reduction in the release of FFAs), and (2) it decreases synthesis of TGs in the liver (attenuating hepatic production of VLDL).…”

Section: Therapeutic Interventionsmentioning

confidence: 99%

High-density lipoprotein (HDL) cholesterol: leveraging practice-based biobank cohorts to characterize clinical and genetic predictors of treatment outcome

Wilke

2010

Pharmacogenomics J

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Over the past decade, large multicenter trials have unequivocally demonstrated that decreasing low density lipoprotein (LDL) cholesterol can reduce both primary and secondary cardiovascular events in patients at risk. However, even in the context of maximal LDL lowering, there remains considerable residual cardiovascular risk. Some of this risk can be attributed to variability in high density lipoprotein (HDL) cholesterol. As such, there is tremendous interest in defining determinants of HDL homeostasis. Risk prediction models are being constructed based upon (1) clinical contributors, (2) known molecular determinants, and (3) the genetic architecture underlying HDL cholesterol levels. To date, however, no single resource has combined these factors within the context of a practice-based dataset. Recently, a number of academic medical centers have begun constructing DNA biobanks linked to secure encrypted versions of their respective electronic medical record. As these biobanks combine resources, the clinical community is in a position to characterize lipid-related treatment outcome on an unprecedented scale.

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Section: Therapeutic Interventionsmentioning

confidence: 99%

High-density lipoprotein (HDL) cholesterol: leveraging practice-based biobank cohorts to characterize clinical and genetic predictors of treatment outcome

Wilke

2010

Pharmacogenomics J

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“…Several subsequent clinical studies established the usage of niacin as a broad-spectrum lipid-regulating medication. Niacin alone or in combination can slow or reverse the progression of atherosclerosis (AS) and reduce cardiovascular event rates and total mortality in patients with hypercholesterolemia and atherosclerotic cardiovascular disease [2, 3]. These effects are generally attributed to favorable actions on the lipoprotein profile, which includes LDL-C reduction and HDL-C elevation.…”

Section: Introductionmentioning

confidence: 99%

Niacin Inhibits Vascular Inflammation via Downregulating Nuclear Transcription Factor-κB Signaling Pathway

Zhang

Zhao

et al. 2014

Mediators of Inflammation

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The study aimed to investigate the effect of niacin on vascular inflammatory lesions in vivo and in vitro as well as its lipid-regulating mechanism. In vivo study revealed that niacin downregulated the levels of inflammatory factors (IL-6 and TNF-α) in plasma, suppressed protein expression of CD68 and NF-κB p65 in arterial wall, and attenuated oxidative stress in guinea pigs that have been fed high fat diet. In vitro study further confirmed that niacin decreased the secretion of IL-6 and TNF-α and inhibited NF-κB p65 and notch1 protein expression in oxLDL-stimulated HUVECs and THP-1 macrophages. Moreover, niacin attenuated oxLDL-induced apoptosis of HUVECs as well. In addition, niacin significantly lessened lipid deposition in arterial wall, increased HDL-C and apoA levels and decreased TG and non-HDL-C levels in plasma, and upregulated the mRNA amount of cholesterol 7α-hydroxylase A1 in liver of guinea pigs. These data suggest for the first time that niacin inhibits vascular inflammation in vivo and in vitro via downregulating NF-κB signaling pathway. Furthermore, niacin also modulates plasma lipid by upregulating the expression of factors involved in the process of reverse cholesterol transport.

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“…Therefore, our study provides a model for investigating the functions and applications of GPR109A. For example, in vascular disease, niacin has been used as an antidyslipidemic drug to prevent and treat atherosclerosis, effects that are mediated by immune cell GPR109A [44, 48, 49]. Our findings in swine will may provide the basis for a more appropriate animal model for atherosclerosis than mouse models because swine is a larger mammal, compared to mice, has more physiological similarities to humans.…”

Section: Discussionmentioning

confidence: 99%

AMP010014A09 in Sus Scrofa Encodes an Analog of G Protein-Coupled Receptor 109A, Which Mediates the Anti-Inflammatory Effects of Beta-Hydroxybutyric Acid

Chen

Feng

et al. 2017

Cell Physiol Biochem

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Background: Hydroxy-carboxylic acid receptor 2 (HCA₂, also called GPR109A) belongs to the G protein-coupled receptor (GPCR) family and is found in humans, rats, mice, hamsters and guinea pigs, but there are almost no reports of this protein in other species. In this investigation, we speculated that AMP010014A09 (AMP+) is a homologue of GPR109A in swine. Methods: To test this hypothesis, the following experiments were designed: monocytes isolated from the peripheral blood of swine were treated with LPS after pretreating with or without β-hydroxybutyric acid (BHBA), and the levels of pro-inflammatory cytokines and inflammatory proteins were assessed. cAMP levels induced by Forskolin in swine testicular (ST) and IPEC-J2 cells were detected with or without BHBA treatment and following silencing or stable transfection of the AMP+ gene. Results: AMP+ in swine exhibited a high level of homology with HM74A in humans and PUMA-G in mice. BHBA inhibited the LPS-induced secretion of the pro-inflammatory cytokines TNF-α, IL-6 and IL-1β and the inflammatory protein COX-2 in monocytes of swine. BHBA suppressed the Forskolin-induced cAMP level increase in ST cells, but failed to inhibit the accumulation of cAMP after the AMP+ gene was silenced with shRNA by transfecting cells with the pGPU6-GFP-Neo-AMP+-sus-392 plasmid. BHBA had no effect on cAMP levels in IPEC-J2 cells, but significantly inhibited the increase in cAMP induced by Forskolin treatment following transfection of the AMP+ gene into IPEC-J2 cells by a lentivirus vector. Conclusion: Our results indicated that AMP+ encodes a G protein-coupled receptor in Sus scrofa that inhibits cAMP levels and mediates anti-inflammatory effects in swine monocytes.

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Niacin therapy in atherosclerosis

Cited by 158 publications

References 45 publications

High-density lipoprotein (HDL) cholesterol: leveraging practice-based biobank cohorts to characterize clinical and genetic predictors of treatment outcome

High-density lipoprotein (HDL) cholesterol: leveraging practice-based biobank cohorts to characterize clinical and genetic predictors of treatment outcome

Niacin Inhibits Vascular Inflammation via Downregulating Nuclear Transcription Factor-κB Signaling Pathway

AMP010014A09 in Sus Scrofa Encodes an Analog of G Protein-Coupled Receptor 109A, Which Mediates the Anti-Inflammatory Effects of Beta-Hydroxybutyric Acid

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