■海洋衍生的omega-3(n-3)多不饱和脂肪酸(PUFA)的临床研究,主要是二十碳五烯酸(EPA)和二十二碳六烯酸(DHA),和植物来源的omega-6(n-6)PUFA亚油酸(LA)对脂蛋白-脂质成分和葡萄糖-胰岛素稳态的影响显示出矛盾的结果,这可以部分解释为女性和男性的差异反应。然而,我们缺乏关于n-3或n-6PUFA消耗增加后心脏代谢风险标志物反应性二态性的数据.
■为了探索补充n-3(EPA+DHA)或n-6(LA)PUFA对循环脂蛋白亚组分的性别特异性反应,标准脂质,载脂蛋白,红细胞膜中的脂肪酸,以及腹型肥胖患者的血糖控制/胰岛素敏感性指标。
这是一项随机双盲交叉研究,有两个7周的干预期,分为9周的冲洗期。雌性(n=16)补充了3g/d的EPADHA(鱼油)或15g/d的LA(红花油),而男性(n=23)接受剂量为4g/d的EPADHA或20g/d的LA。在禁食的血液样本中,我们测量了脂蛋白颗粒亚类,标准脂质,载脂蛋白,脂肪酸谱,和血糖控制/胰岛素敏感性的标志物。
■总高密度脂蛋白在n-3后相对变化分数的性别差异显着(女性/男性:-11%*/-3.3%,p=0.036;*:显著的性别内变化),高密度脂蛋白粒径(+2.1%*/-0.1%,p=0.045),和花生四烯酸(-8.3%*/-12%*,p=0.012),在总共n-6之后(+37%*/+2.1%,p=0.041)和小的极低密度脂蛋白(+97%*/+14%,p=0.021),和脂蛋白(a)(-16%*/+0.1%,p=0.028)。葡萄糖-胰岛素稳态的循环标志物在n-3后存在显着差异(女性/男性:-2.1%/3.9%*,p=0.029),胰岛素(-31%*/+16%,p<0.001),胰岛素C肽(-12%*/+13%*,p=0.001),胰岛素抵抗指数2的稳态模型评估(-12%*/+14%*,p=0.001)和胰岛素敏感性指数2(+14%*/-12%*,p=0.001),和定量胰岛素敏感性检查指数(+4.9%*/-3.4%*,p<0.001)。
■我们发现高剂量n-3(而不是n-6)补充后,在血糖控制/胰岛素敏感性的循环标志物中具有性别特异性反应,女性有所改善,但男性恶化。这可能部分与我们在n-3干预后在脂蛋白脂质分布的几个组成部分中观察到的性别差异有关。
■https://clinicaltrials.gov/,标识符[NCT02647333]。
UNASSIGNED: Clinical studies on effects of marine-derived omega-3 (n-3) polyunsaturated fatty acids (PUFAs), mainly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), and the plant-derived omega-6 (n-6) PUFA linoleic acid (LA) on lipoprotein-lipid components and glucose-insulin homeostasis have shown conflicting results, which may partly be explained by differential responses in females and males. However, we have lacked data on sexual dimorphism in the response of cardiometabolic risk markers following increased consumption of n-3 or n-6 PUFAs.
UNASSIGNED: To explore sex-specific responses after n-3 (EPA + DHA) or n-6 (LA) PUFA supplementation on circulating lipoprotein subfractions, standard lipids, apolipoproteins, fatty acids in red blood cell membranes, and markers of glycemic control/insulin sensitivity among people with abdominal obesity.
UNASSIGNED: This was a randomized double-blind crossover study with two 7-week intervention periods separated by a 9-week washout phase. Females (n = 16) were supplemented with 3 g/d of EPA + DHA (fish oil) or 15 g/d of LA (safflower oil), while males (n = 23) received a dose of 4 g/d of EPA + DHA or 20 g/d of LA. In fasting blood samples, we measured lipoprotein particle subclasses, standard lipids, apolipoproteins, fatty acid profiles, and markers of glycemic control/insulin sensitivity.
UNASSIGNED: The between-sex difference in relative change scores was significant after n-3 for total high-density lipoproteins (females/males: -11%*/-3.3%, p = 0.036; *: significant within-sex change), high-density lipoprotein particle size (+2.1%*/-0.1%, p = 0.045), and arachidonic acid (-8.3%*/-12%*, p = 0.012), and after n-6 for total (+37%*/+2.1%, p = 0.041) and small very-low-density lipoproteins (+97%*/+14%, p = 0.021), and lipoprotein (a) (-16%*/+0.1%, p = 0.028). Circulating markers of glucose-insulin homeostasis differed significantly after n-3 for glucose (females/males: -2.1%/+3.9%*, p = 0.029), insulin (-31%*/+16%, p < 0.001), insulin C-peptide (-12%*/+13%*, p = 0.001), homeostasis model assessment of insulin resistance index 2 (-12%*/+14%*, p = 0.001) and insulin sensitivity index 2 (+14%*/-12%*, p = 0.001), and quantitative insulin sensitivity check index (+4.9%*/-3.4%*, p < 0.001).
UNASSIGNED: We found sex-specific responses after high-dose n-3 (but not n-6) supplementation in circulating markers of glycemic control/insulin sensitivity, which improved in females but worsened in males. This may partly be related to the sex differences we observed in several components of the lipoprotein-lipid profile following the n-3 intervention.
UNASSIGNED: https://clinicaltrials.gov/, identifier [NCT02647333].