关键词: Lp(a) metabolism apolipoprotein fructose glucose nutrition

Mesh : Humans Female Male Middle Aged Obesity / metabolism blood Overweight / blood metabolism Lipoprotein(a) / blood Adult Sugar-Sweetened Beverages Diet Double-Blind Method Fructose / administration & dosage

来  源:   DOI:10.1016/j.jlr.2024.100588   PDF(Pubmed)

Abstract:
Lipoprotein(a) [Lp(a)] contributes to cardiovascular disease risk. A genetically determined size polymorphism in apolipoprotein(a) [apo(a)], determined by the number of Kringle (K) repeats, inversely regulates Lp(a) levels. Nongenetic factors including dietary saturated fat influence Lp(a) levels. However, less is known about the effects of carbohydrates including dietary sugars. In this double-blind, parallel arm study among 32 overweight/obese adults, we investigated the effect of consuming glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks on Lp(a) level and assessed the role of the apo(a) size polymorphism. The mean (±SD) age of participants was 54 ± 8 years, 50% were women, and 75% were of European descent. Following the 10-week intervention, Lp(a) level was reduced by an average (±SEM) of -13.2% ± 4.3% in all participants (P = 0.005); -15.3% ± 7.8% in the 15 participants who consumed glucose (P = 0.07); and -11.3% ± 4.5% in the 17 participants who consumed fructose (P = 0.02), without any significant difference in the effect between the two sugar groups. Relative changes in Lp(a) levels were similar across subgroups of lower versus higher baseline Lp(a) level or carrier versus noncarrier of an atherogenic small (≤22K) apo(a) size. In contrast, LDL-C increased. In conclusion, in older, overweight/obese adults, consuming sugar-sweetened beverages reduced Lp(a) levels by ∼13% independently of apo(a) size variability and the type of sugar consumed. The Lp(a) response was opposite to that of LDL-C and triglyceride concentrations. These findings suggest that metabolic pathways might impact Lp(a) levels.
摘要:
脂蛋白(a)[Lp(a)]是心血管疾病的危险因素。载脂蛋白(a)[apo(a)]基因的大小多态性,由Kringle(K)重复的数量决定,反向调节Lp(a)水平。包括膳食饱和脂肪在内的非遗传因素影响Lp(a)水平。然而,人们对包括膳食糖在内的碳水化合物的影响知之甚少。在这个双盲中,32名超重/肥胖成年人的平行臂研究,我们调查了在10周内摄入能提供25%能量需求的葡萄糖或果糖甜味饮料对Lp(a)水平的影响,并评估了apo(a)大小多态性的作用.参与者的平均(±SD)年龄为54±8岁,50%是女性,75%是欧洲人后裔.在为期10周的干预结束时,在所有参与者中,Lp(a)水平平均降低了-13.2%±4.3%(p=0.005);在消耗葡萄糖的15名参与者中降低了-15.3%±7.8%(p=0.07);在消耗果糖的17名参与者中降低了-11.3%±4.5%(p=0.02),两个糖组之间的效果没有任何显着差异。Lp(a)水平的相对变化在低基线Lp(a)水平和高基线Lp(a)水平或动脉粥样硬化小(≤22K)apo(a)大小的携带者和非携带者之间相似。相比之下,LDL-C升高。总之,在较老的时候,超重/肥胖的成年人,食用含糖饮料可将Lp(a)水平降低13%,而与apo(a)大小变异性和消耗的糖类型无关。Lp(a)反应与LDL-C和甘油三酸酯浓度相反。这些发现表明代谢途径可能影响Lp(a)水平。
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