Citation
Lauring, Brett, et al. "Niacin Lipid Efficacy Is Independent of Both the Niacin Receptor GPR109A and Free Fatty Acid Suppression." Science Translational Medicine, vol. 4, no. 148, 2012, pp. 148ra115.
Lauring B, Taggart AK, Tata JR, et al. Niacin lipid efficacy is independent of both the niacin receptor GPR109A and free fatty acid suppression. Sci Transl Med. 2012;4(148):148ra115.
Lauring, B., Taggart, A. K., Tata, J. R., Dunbar, R., Caro, L., Cheng, K., Chin, J., Colletti, S. L., Cote, J., Khalilieh, S., Liu, J., Luo, W. L., Maclean, A. A., Peterson, L. B., Polis, A. B., Sirah, W., Wu, T. J., Liu, X., Jin, L., ... Plump, A. (2012). Niacin lipid efficacy is independent of both the niacin receptor GPR109A and free fatty acid suppression. Science Translational Medicine, 4(148), 148ra115. https://doi.org/10.1126/scitranslmed.3003877
Lauring B, et al. Niacin Lipid Efficacy Is Independent of Both the Niacin Receptor GPR109A and Free Fatty Acid Suppression. Sci Transl Med. 2012 Aug 22;4(148):148ra115. PubMed PMID: 22914621.
TY - JOUR
T1 - Niacin lipid efficacy is independent of both the niacin receptor GPR109A and free fatty acid suppression.
AU - Lauring,Brett,
AU - Taggart,Andrew K P,
AU - Tata,James R,
AU - Dunbar,Richard,
AU - Caro,Luzelena,
AU - Cheng,Kang,
AU - Chin,Jayne,
AU - Colletti,Steven L,
AU - Cote,Josee,
AU - Khalilieh,Sauzanne,
AU - Liu,Jiajun,
AU - Luo,Wen-Lin,
AU - Maclean,Alexandra A,
AU - Peterson,Laurence B,
AU - Polis,Adam B,
AU - Sirah,Waheeda,
AU - Wu,Tsuei-Ju,
AU - Liu,Xuan,
AU - Jin,Lan,
AU - Wu,Kenneth,
AU - Boatman,P Douglas,
AU - Semple,Graeme,
AU - Behan,Dominic P,
AU - Connolly,Daniel T,
AU - Lai,Eseng,
AU - Wagner,John A,
AU - Wright,Samuel D,
AU - Cuffie,Cynthia,
AU - Mitchel,Yale B,
AU - Rader,Daniel J,
AU - Paolini,John F,
AU - Waters,M Gerard,
AU - Plump,Andrew,
PY - 2012/8/24/entrez
PY - 2012/8/24/pubmed
PY - 2013/5/25/medline
SP - 148ra115
EP - 148ra115
JF - Science translational medicine
JO - Sci Transl Med
VL - 4
IS - 148
N2 - Nicotinic acid (niacin) induces beneficial changes in serum lipoproteins and has been associated with beneficial cardiovascular effects. Niacin reduces low-density lipoprotein, increases high-density lipoprotein, and decreases triglycerides. It is well established that activation of the seven-transmembrane G(i)-coupled receptor GPR109A on Langerhans cells results in release of prostaglandin D₂, which mediates the well-known flushing side effect of niacin. Niacin activation of GPR109A on adipocytes also mediates the transient reduction of plasma free fatty acid (FFA) levels characteristic of niacin, which has been long hypothesized to be the mechanism underlying the changes in the serum lipid profile. We tested this "FFA hypothesis" and the hypothesis that niacin lipid efficacy is mediated via GPR109A by dosing mice lacking GPR109A with niacin and testing two novel, full GPR109A agonists, MK-1903 and SCH900271, in three human clinical trials. In mice, the absence of GPR109A had no effect on niacin's lipid efficacy despite complete abrogation of the anti-lipolytic effect. Both MK-1903 and SCH900271 lowered FFAs acutely in humans; however, neither had the expected effects on serum lipids. Chronic FFA suppression was not sustainable via GPR109A agonism with niacin, MK-1903, or SCH900271. We conclude that the GPR109A receptor does not mediate niacin's lipid efficacy, challenging the long-standing FFA hypothesis.
SN - 1946-6242
UR - https://www.unboundmedicine.com/medline/citation/22914621/Niacin_lipid_efficacy_is_independent_of_both_the_niacin_receptor_GPR109A_and_free_fatty_acid_suppression_
L2 - https:///www.science.org/doi/10.1126/scitranslmed.3003877?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed
DB - PRIME
DP - Unbound Medicine
ER -
