Abstract
PURPOSE OF REVIEW
This review focuses on the current understanding of the physiological mechanisms of action of niacin on lipid metabolism and atherosclerosis.
RECENT FINDINGS
Emerging findings indicate that niacin decreases hepatic triglyceride synthesis and subsequent VLDL/LDL secretion by directly and noncompetitively inhibiting hepatocyte diacylglycerol acyltransferase 2. Recent studies in mice lacking niacin receptor GPR109A and human clinical trials with GPR109A agonists disproved the long believed hypothesis of adipocyte triglyceride lipolysis as the mechanism for niacin's effect on serum lipids. Niacin, through inhibiting hepatocyte surface expression of β-chain ATP synthase, inhibits the removal of HDL-apolipoprotein (apo) AI resulting in increased apoAI-containing HDL particles. Additional recent findings suggest that niacin by increasing hepatic ATP-binding cassette transporter A1-mediated apoAI lipidation increases HDL biogenesis, thus stabilizing circulation of newly secreted apoAI. New concepts have also emerged on lipid-independent actions of niacin on vascular endothelial oxidative and inflammatory events, myeloperoxidase release from neutrophils and its impact on HDL function, and GPR109A-mediated macrophage inflammatory events involved in atherosclerosis.
SUMMARY
Recent advances have provided physiological mechanisms of action of niacin on lipid metabolism and atherosclerosis. Better understanding of niacin's actions on multiple tissues and targets may be helpful in designing combination therapy and new treatment strategies for atherosclerosis.
Pub Type(s)
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Review
TY - JOUR
T1 - Recent advances in niacin and lipid metabolism.
AU - Kamanna,Vaijinath S,
AU - Ganji,Shobha H,
AU - Kashyap,Moti L,
PY - 2013/4/27/entrez
PY - 2013/4/27/pubmed
PY - 2014/5/3/medline
SP - 239
EP - 45
JF - Current opinion in lipidology
JO - Curr Opin Lipidol
VL - 24
IS - 3
N2 - PURPOSE OF REVIEW: This review focuses on the current understanding of the physiological mechanisms of action of niacin on lipid metabolism and atherosclerosis. RECENT FINDINGS: Emerging findings indicate that niacin decreases hepatic triglyceride synthesis and subsequent VLDL/LDL secretion by directly and noncompetitively inhibiting hepatocyte diacylglycerol acyltransferase 2. Recent studies in mice lacking niacin receptor GPR109A and human clinical trials with GPR109A agonists disproved the long believed hypothesis of adipocyte triglyceride lipolysis as the mechanism for niacin's effect on serum lipids. Niacin, through inhibiting hepatocyte surface expression of β-chain ATP synthase, inhibits the removal of HDL-apolipoprotein (apo) AI resulting in increased apoAI-containing HDL particles. Additional recent findings suggest that niacin by increasing hepatic ATP-binding cassette transporter A1-mediated apoAI lipidation increases HDL biogenesis, thus stabilizing circulation of newly secreted apoAI. New concepts have also emerged on lipid-independent actions of niacin on vascular endothelial oxidative and inflammatory events, myeloperoxidase release from neutrophils and its impact on HDL function, and GPR109A-mediated macrophage inflammatory events involved in atherosclerosis. SUMMARY: Recent advances have provided physiological mechanisms of action of niacin on lipid metabolism and atherosclerosis. Better understanding of niacin's actions on multiple tissues and targets may be helpful in designing combination therapy and new treatment strategies for atherosclerosis.
SN - 1473-6535
UR - https://www.unboundmedicine.com/medline/citation/23619367/Recent_advances_in_niacin_and_lipid_metabolism_
L2 - https://doi.org/10.1097/MOL.0b013e3283613a68
DB - PRIME
DP - Unbound Medicine
ER -
