Department of Food and Human Nutritional Sciences, University of Manitoba, Winnipeg, Manitoba, Canada.
Richardson Centre for Functional Foods and Nutraceuticals, University of Manitoba, Winnipeg, Manitoba, Canada.
J Nutr. 2019 Oct 1;149(10):1749-1756. doi: 10.1093/jn/nxz136.
Different fatty acids (FAs) can vary in their obesogenic effect, and genetic makeup can contribute to fat deposition in response to dietary FA composition. However, the antiobesogenic effects of the interactions between dietary MUFAs and genetics have scarcely been tested in intervention studies.
We evaluated the overall (primary outcome) and genetically modulated (secondary outcome) response in body weight and fat mass to different levels of MUFA consumption.
In the Canola Oil Multicenter Intervention Trial II, a randomized, crossover, isocaloric, controlled-feeding multicenter trial, 44 men and 71 women with a mean age of 44 y and an increased waist circumference (men ∼108 cm and women ∼102 cm) consumed each of 3 oils for 6 wk, separated by four 12-wk washout periods. Oils included 2 high-MUFA oils-conventional canola and high-oleic canola (<7% SFAs, >65% MUFAs)-and 1 low-MUFA/high-SFA oil blend (40.2% SFAs, 22.0% MUFAs). Body fat was measured using DXA. Five candidate single-nucleotide polymorphisms (SNPs) were genotyped using qualitative PCR. Data were analyzed using a repeated measures mixed model.
No significant differences were observed in adiposity measures following the consumption of either high-MUFA diet compared with the low-MUFA/high-SFA treatment. However, when stratified by genotype, 3 SNPs within lipoprotein lipase (LPL), adiponectin, and apoE genes influenced, separately, fat mass changes in response to treatment (n = 101). Mainly, the LPL rs13702-CC genotype was associated with lower visceral fat (high-MUFA: -216.2 ± 58.6 g; low-MUFA: 17.2 ± 81.1 g; P = 0.017) and android fat mass (high-MUFA: -267.3 ± 76.4 g; low-MUFA: -21.7 ± 102.2 g; P = 0.037) following average consumption of the 2 high-MUFA diets.
Common variants in LPL, adiponectin, and apoE genes modulated body fat mass response to dietary MUFAs in an isocaloric diet in adults with abdominal obesity. These findings might eventually help in developing personalized dietary recommendations for weight control. The trial was registered at clinicaltrials.gov as NCT02029833 (https://www.clinicaltrials.gov/ct2/show/NCT02029833?cond=NCT02029833&rank=1).
不同的脂肪酸(FAs)在肥胖效应方面可能存在差异,遗传构成可能导致脂肪在饮食 FA 组成的影响下沉积。然而,饮食 MUFA 与遗传之间相互作用的抗肥胖作用在干预研究中几乎没有得到检验。
我们评估了不同 MUFA 摄入量对体重和体脂肪的总体(主要结果)和遗传调节(次要结果)反应。
在菜籽油多中心干预试验 II 中,一项随机、交叉、等热量、对照喂养的多中心试验中,44 名男性和 71 名女性,平均年龄 44 岁,腰围增加(男性约 108 厘米,女性约 102 厘米),每人食用 3 种油 6 周,每种油之间有 4 个 12 周的洗脱期。油包括 2 种高 MUFA 油——传统菜籽油和高油酸菜籽油(<7%SFAs,>65%MUFA)和 1 种低 MUFA/高 SFA 油混合物(40.2%SFAs,22.0%MUFA)。使用 DXA 测量体脂肪。使用定性 PCR 对 5 个候选单核苷酸多态性(SNPs)进行基因分型。使用重复测量混合模型进行数据分析。
与低 MUFA/高 SFA 处理相比,高 MUFA 饮食的摄入并没有观察到肥胖指标的显著差异。然而,当按基因型分层时,脂蛋白脂肪酶(LPL)、脂联素和载脂蛋白 E 基因中的 3 个 SNP 分别影响了治疗反应时的脂肪量变化(n=101)。主要是,LPL rs13702-CC 基因型与内脏脂肪(高 MUFA:-216.2±58.6g;低 MUFA:17.2±81.1g;P=0.017)和腹型脂肪质量(高 MUFA:-267.3±76.4g;低 MUFA:-21.7±102.2g;P=0.037)的降低有关,平均食用两种高 MUFA 饮食后。
LPL、脂联素和载脂蛋白 E 基因的常见变异在腹部肥胖成年人的等热量饮食中调节了膳食 MUFA 对体脂肪量的反应。这些发现最终可能有助于制定个性化的饮食建议来控制体重。该试验在 clinicaltrials.gov 上注册为 NCT02029833(https://www.clinicaltrials.gov/ct2/show/NCT02029833?cond=NCT02029833&rank=1)。