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Recent advances in niacin and lipid metabolism

机译：烟酸和脂质代谢的最新进展

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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 b-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.
机译：综述的目的这篇综述着重于对烟酸对脂质代谢和动脉粥样硬化作用的生理机制的当前理解。最新发现新发现表明，烟酸通过直接和非竞争性抑制肝细胞二酰基甘油酰基转移酶2降低了肝甘油三酸酯的合成和随后的VLDL / LDL分泌。最近在缺乏烟酸受体GPR109A的小鼠中进行的研究以及有关GPR109A激动剂的人体临床试验均不支持长期以来认为的脂肪细胞甘油三酸酯假说脂解作为烟酸对血脂的作用机理。烟酸通过抑制b链ATP合酶的肝细胞表面表达，抑制了HDL-载脂蛋白（apo）AI的去除，从而导致含apoAI的HDL颗粒增加。最近的其他发现表明，烟酸通过增加肝脏ATP结合盒转运蛋白A1介导的apoAI脂质化而增加HDL生物发生，从而稳定新分泌的apoAI的循环。关于烟酸对血管内皮氧化和炎性事件的脂质非依赖性作用，嗜中性粒细胞释放的髓过氧化物酶及其对HDL功能的影响以及与动脉粥样硬化有关的GPR109A介导的巨噬细胞炎性事件的新概念也已经出现。总结最近的进展提供了烟酸对脂质代谢和动脉粥样硬化作用的生理机制。更好地了解烟酸对多种组织和靶标的作用可能有助于设计组合疗法和动脉粥样硬化的新治疗策略。

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