脂蛋白(a)与饮食的影响:重新评估的时候了。
Lipoprotein(a) and Effects of Diet: Time for Reassessment.
作者信息
Enkhmaa Byambaa, Berglund Lars
机构信息
Department of Internal Medicine, School of Medicine, University of California Davis, One Shields Avenue, Davis, CA 95616, USA.
出版信息
Nutrients. 2025 May 19;17(10):1714. doi: 10.3390/nu17101714.
Dietary modification is a critical tool in the prevention of cardiovascular disease (CVD). While the role of saturated fat (SFA) intake is well established in affecting LDL cholesterol concentrations, diet impacts on lipoprotein(a) (Lp(a)) have been less studied. Lp(a) is a prevalent, strong, and highly heritable risk factor for CVD and a therapeutic target for CVD risk management. While significant insights have been made into the genetic regulation of Lp(a), our understanding of any metabolic impact on Lp(a) by other factors, including diets, is limited. For many years, Lp(a) was not considered to be subject to dietary regulation, but there is now clear evidence of a dietary impact, in particular variability in SFA intake, on Lp(a) concentrations. The present narrative review aims to provide an updated view on dietary regulation of Lp(a), moving beyond studies testing the effect of reducing SFA intake, to include new evidence from clinical trials on the impact of an increased sugar intake and ketogenic diets. In addition to describing an opposite effect of SFA on Lp(a) and LDL cholesterol concentrations, with a rise in Lp(a) during a reduced SFA intake, this review also provides new data on the role of apolipoprotein(a) size polymorphism, a major genetic regulator of Lp(a) concentrations. Beyond an impact on Lp(a) concentrations, the extent to which diet might impact Lp(a)'s molecular and metabolic properties including its lipidomic composition remains unknown. Taken together, evidence shows the presence of a dietary modulation of Lp(a) beyond its genetic control and points to the need to better understand Lp(a)'s cardiovascular risk factor properties, including metabolomics/lipidomics characteristics. This also raises the issue whether diet should be a component of elevated Lp(a) management, and this needs to be addressed in future studies.
饮食调整是预防心血管疾病(CVD)的关键手段。虽然饱和脂肪(SFA)摄入量对低密度脂蛋白胆固醇浓度的影响已得到充分证实,但饮食对脂蛋白(a)(Lp(a))的影响研究较少。Lp(a)是一种常见、强效且高度可遗传的心血管疾病风险因素,也是心血管疾病风险管理的治疗靶点。尽管在Lp(a)的基因调控方面已取得重大进展,但我们对包括饮食在内的其他因素对Lp(a)的任何代谢影响的了解仍然有限。多年来,Lp(a)一直被认为不受饮食调节,但现在有明确证据表明饮食,特别是SFA摄入量的变化,会对Lp(a)浓度产生影响。本叙述性综述旨在提供关于Lp(a)饮食调节的最新观点,超越测试降低SFA摄入量效果的研究,纳入来自临床试验的关于糖摄入量增加和生酮饮食影响的新证据。除了描述SFA对Lp(a)和低密度脂蛋白胆固醇浓度的相反影响,即SFA摄入量减少时Lp(a)升高,本综述还提供了关于载脂蛋白(a)大小多态性作用的新数据,载脂蛋白(a)大小多态性是Lp(a)浓度的主要基因调节因子。除了对Lp(a)浓度的影响外,饮食对Lp(a)的分子和代谢特性(包括其脂质组学组成)的影响程度仍然未知。综合来看,证据表明存在超出基因控制的Lp(a)饮食调节,并指出需要更好地了解Lp(a)的心血管疾病风险因素特性,包括代谢组学/脂质组学特征。这也引发了饮食是否应成为Lp(a)升高管理的一部分的问题,这需要在未来的研究中加以解决。