Effects of niacin and chromium on the expression of ATP-binding cassette transporter A1 and apolipoprotein A-1 genes in HepG2 cells.

@article{Siripurkpong2009EffectsON,
  title={Effects of niacin and chromium on the expression of ATP-binding cassette transporter A1 and apolipoprotein A-1 genes in HepG2 cells.},
  author={Pilaiwan Siripurkpong and Kesara Na-Bangchang},
  journal={The Journal of nutritional biochemistry},
  year={2009},
  volume={20 4},
  pages={
          261-8
        }
}
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16 Citations
Highly Influential Citations
2
Background Citations
3
Methods Citations
1
Results Citations
1

16 Citations

Nicotinic acid induces apolipoprotein A-I gene expression in HepG2 and Caco-2 cell lines.
Nicotinic acid, lauric acid and kaempferol abolish ATP-binding cassettetransporter subfamily A member 1 (ABCA1) down-regulation by TNF-?in hepatocarcinoma HepG2 cell line.
TLDR
This study successfully profiled that all the three antioxidants were able to alleviate the downregulatory effect of TNF-α on ABCA1 transcript level in HepG2 cells.
Effects of nicotinic acid on gene expression: potential mechanisms and implications for wanted and unwanted effects of the lipid-lowering drug.
TLDR
NA effects on gene expression provide new insights into previously unexplained NA effects, such as FFA-independent lipid-lowering effects, FFA rebound, and insulin resistance observed in clinics during NA treatment.
Protective role of coenzyme Q10, riboflavin, niacin, selenium (CoRNS) and Emblica officinalis on cardiac abnormalities in experimental atherosclerosis
The high-fat high-fructose hamster as an animal model for niacin's biological activities in humans.
Therapeutic Interventions to Enhance Apolipoprotein A-I-Mediated Cardioprotection
TLDR
The results of recent phase III clinical trials utilizing a cholesterol ester transfer protein (CETP) inhibitor to increase HDL-C levels in hypoalphalipoproteinaemia have shown that this approach of elevating HDL- C levels is insufficient to combat atherosclerosis and reduce the risk of cardiovascular disease.
Intestinal lymphatic HDL miR‐223 and ApoA‐I are reduced during insulin resistance and restored with niacin
  • R. MangatF. Borthwick S. Proctor
  • Biology
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • 2018
TLDR
Altered intestinal lymphatic HDL‐ApoA‐I and miR‐223 metabolism in IR and modulation by niacin may provide insight into the intestinal‐mediated regulation of the reverse cholesterol transport pathway.
Plant-Based Foods as a Source of Lipotropes for Human Nutrition: A Survey of In Vivo Studies
TLDR
The exhaustive review of rat studies investigating phytochemical effect on hepatic lipid metabolism suggests that some fatty acids, acetic acid, melatonin, phytic acid, some fiber compounds, oligofructose, resistant starch, some phenolic acids, flavonoids, lignans, stilbenes, curcumin, saponins, coumarin, some plant extracts, and some solid foods may be lipotropic.
Brothers in Arms: ABCA1- and ABCG1-Mediated Cholesterol Efflux as Promising Targets in Cardiovascular Disease Treatment
TLDR
A systematic review discusses the molecular mechanisms relevant for RCT and ABCA1 and ABCG1 function, followed by a critical overview of potential pharmacological strategies with small molecules to enhance cellular cholesterol efflux and RCT.
Nicotinic Acid Accelerates HDL Cholesteryl Ester Turnover in Obese Insulin-Resistant Dogs
TLDR
NA decreased HDL cholesterol but promoted cholesterol efflux and esterification, leading to improved reverse cholesterol transport, highlighting the CETP-independent effects of NA in changes of plasma lipid profile.
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References

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Effect of chromium on apolipoprotein A-I expression in HepG2 cells.
ATP-binding Cassette Transporter A1 (ABCA1) Functions as a Cholesterol Efflux Regulatory Protein*
TLDR
The data suggest that the binding of apoA-I to ABCA1 leads to the formation of phospholipid-apoA- I complexes, which subsequently promote cholesterol efflux in an autocrine or paracrine fashion.
Niacin decreases removal of high-density lipoprotein apolipoprotein A-I but not cholesterol ester by Hep G2 cells. Implication for reverse cholesterol transport.
TLDR
Data indicate a novel mechanism whereby niacin selectively decreases hepatic removal of HDL apoA-I but not cholesterol esters, thereby increasing the capacity of retained apo A-I to augment reverse cholesterol transport.
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.
ABCA1-dependent lipid efflux to apolipoprotein A-I mediates HDL particle formation and decreases VLDL secretion from murine hepatocytes Published, JLR Papers in Press, March 1, 2004. DOI 10.1194/jlr.M300529-JLR200
TLDR
A major role for hepatocyte ABCA1 is supported in generating a critical pool of HDL precursor particles that enhance further HDL generation and passive cholesterol mobilization in the periphery and diversion of hepatocyte cholesterol into the “reverse” cholesterol transport pathway diminishes cholesterol availability for apoB-containing lipoprotein secretion by the liver.
Identification of Sterol-independent Regulatory Elements in the Human ATP-binding Cassette Transporter A1 Promoter
TLDR
A functional complex of cis-elements within the proximal human ABCA1 promoter associated with the transcription factors Sp1/3, upstream stimulatory factors 1 and 2, and hepatic nuclear factor 1α has been characterized, which allows a subtle tissue-specific regulation ofABCA1 gene expression.
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TLDR
Current approaches to increasing HDL to determine the efficacy of HDL in reducing atherosclerosis involve acute HDL therapy with infusions of apo-I or apoA-I mimetic peptides and chronic long-term therapy with selective agents to increase HDL, including CETP inhibitors.
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A PPARγ-LXR-ABCA1 Pathway in Macrophages Is Involved in Cholesterol Efflux and Atherogenesis
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