长期禁食的高密度脂蛋白胆固醇外流能力和胆固醇负荷能力:一项针对健康人的前瞻性单臂干预研究提供的证据

IF 4.9 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
Franziska Grundler , Marcella Palumbo , Maria Pia Adorni , Francesca Zimetti , Bianca Papotti , Dietmar Plonné , Alfred Holley , Robin Mesnage , Massimiliano Ruscica , Françoise Wilhelmi de Toledo
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引用次数: 0

摘要

背景和目的长期禁食(LF)正逐渐成为一种非药物方法,用于调节与动脉粥样硬化性心血管疾病(ASCVD)发展相关的风险因素。然而,防止动脉粥样硬化性心血管疾病更多地与高密度脂蛋白(HDL)的功能而不是其血浆水平有关。我们的前瞻性干预研究侧重于脂蛋白在调节外周细胞胆固醇稳态方面的功能特性,并探讨低密度脂蛋白如何影响脂蛋白亚类的组成。为此,我们研究了低密度脂蛋白对高密度脂蛋白胆固醇外排能力(CEC)和血清胆固醇负荷能力(CLC)的影响。32名受试者在重新摄入食物一个月后接受了随访检查。空腹降低了甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)和高密度脂蛋白胆固醇(HDL-C)。极低密度脂蛋白胆固醇(VLDL-C)和低密度脂蛋白胆固醇(LDL3-C)在随访中持续下降。只有高密度脂蛋白胆固醇(尤其是高密度脂蛋白2-C水平)在随访中有所增加。总 HDL-CEC 在 LF 期间下降,在随访时高于基线。空腹会降低 ATP 结合盒 (ABC)A1 介导的 HDL-CEC,而 ABCG1 介导的 HDL-CEC 则不受影响。随访时,水扩散增加。结论 低脂蛋白不仅能维持脂蛋白的功能,还能促使致动脉粥样硬化风险发生有利的转变,这种转变甚至在重新引入食物后仍然存在。这进一步强调了在进行传统血脂测量的同时考虑高密度脂蛋白功能的重要性,以了解低密度脂蛋白等非药物干预措施在促进心血管预防和健康方面的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

HDL cholesterol efflux capacity and cholesterol loading capacity in long-term fasting: Evidence from a prospective, single-arm interventional study in healthy individuals

HDL cholesterol efflux capacity and cholesterol loading capacity in long-term fasting: Evidence from a prospective, single-arm interventional study in healthy individuals

Background and aims

Long-term fasting (LF) is increasingly emerging as a non-pharmacological approach to modulate risk factors associated with the development of atherosclerotic cardiovascular diseases (ASCVD). However, protection from ASCVD is more tied to the functionality of high-density lipoprotein (HDL) than its plasma levels. Our prospective interventional study focuses on the functional properties of lipoproteins in modulating cholesterol homeostasis on peripheral cells and examines how LF may influence this and lipoprotein subclass composition. For that purpose, we investigated its impact on HDL-cholesterol efflux capacity (CEC), and on serum cholesterol loading capacity (CLC).

Methods

Forty healthy subjects (50 % females) underwent medically supervised 9-day fasting (250 kcal/day) in a specialised facility. Thirty-two subjects had a follow-up examination after one month of food reintroduction.

Results

LF was well tolerated and increased self-reported energy levels. Fasting reduced triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and HDL cholesterol (HDL-C). Very-low-density lipoprotein cholesterol (VLDL-C) and LDL3-C showed sustained reductions at follow-up. Only HDL-C, specifically HDL2-C levels, increased at follow-up. Total HDL-CEC decreased during LF and increased above baseline at follow-up. Fasting decreased ATP binding cassette (ABC)A1-mediated HDL-CEC whereas ABCG1-mediated HDL-CEC remained unaffected. Aqueous diffusion increased at follow up. LF decreased serum CLC and then returned to baseline levels.

Conclusions

LF not only maintains lipoprotein functionality but also contributes to a favorable shift in the atherogenic risk profile, which persists even after food reintroduction. This further emphasizes the importance of considering HDL functionality alongside traditional lipid measurements to understand the potential for non-pharmacological interventions like LF to promote cardiovascular prevention and health.

Trial registration number

NCT05031598.

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来源期刊
Atherosclerosis
Atherosclerosis 医学-外周血管病
CiteScore
9.80
自引率
3.80%
发文量
1269
审稿时长
36 days
期刊介绍: Atherosclerosis has an open access mirror journal Atherosclerosis: X, sharing the same aims and scope, editorial team, submission system and rigorous peer review. Atherosclerosis brings together, from all sources, papers concerned with investigation on atherosclerosis, its risk factors and clinical manifestations. Atherosclerosis covers basic and translational, clinical and population research approaches to arterial and vascular biology and disease, as well as their risk factors including: disturbances of lipid and lipoprotein metabolism, diabetes and hypertension, thrombosis, and inflammation. The Editors are interested in original or review papers dealing with the pathogenesis, environmental, genetic and epigenetic basis, diagnosis or treatment of atherosclerosis and related diseases as well as their risk factors.
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