Rasaei Niloufar, Fatemi Seyedeh Fatemeh, Gholami Fatemeh, Samadi Mahsa, Mohammadian Mohammad Keshavarz, Daneshzad Elnaz, Mirzaei Khadijeh
Micronutrient Research Center, Research Institute for Endocrine Disorders, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Department of Community Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences (TUMS), Tehran, Iran.
BMC Med Genomics. 2025 Jan 21;18(1):16. doi: 10.1186/s12920-024-02066-4.
The growth in obesity and rates of abdominal obesity in developing countries is due to the dietary transition, meaning a shift from traditional, fiber-rich diets to Westernized diets high in processed foods, sugars, and unhealthy fats. Environmental changes, such as improving the quality of dietary fat consumed, may be useful in preventing or mitigating the obesity or unhealthy obesity phenotype in individuals with a genetic predisposition, although this has not yet been confirmed. Therefore, in this study, we investigated how dietary fat quality indices with metabolically healthy obesity (MHO) or metabolically unhealthy obesity (MUO) based on the Karelis criterion interact with genetic susceptibility in Iranian female adults.
In the current cross-sectional study, 279 women with overweight or obesity participated. Dietary intake was assessed using a 147-item food frequency questionnaire and dietary fat quality was assessed using the cholesterol-saturated fat index (CSI) and the ratio of omega-6/omega-3 (N6/N3) essential fatty acids. Three single nucleotide polymorphisms-MC4R (rs17782313), CAV-1 (rs3807992), and Cry-1(rs2287161) were genotyped by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique and were combined to produce the genetic risk score (GRS). Body composition was evaluated using a multi-frequency bioelectrical impedance analyzer. Participants were divided into MHO or MUO phenotypes after the metabolic risk assessment based on the Karelis criteria.
We found significant interactions between GRS and N6/N3 in the adjusted model controlling for confounding factors (age, body mass index, energy, and physical activity) (β = 2.26, 95% CI: 0.008 to 4.52, P = 0.049). In addition, we discovered marginally significant interactions between GRS and N6/N3 in crude (β = 1.92, 95% CI: -0.06 to 3.91, P = 0.058) and adjusted (age and energy) (β = 2.00, 95% CI: -0.05 to 4.05, P = 0.057) models on the MUH obesity phenotype. However, no significant interactions between GRS and CSI were shown in both crude and adjusted models.
This study highlights the importance of personalized nutrition and recommends further study of widely varying fat intake based on the findings on gene-N6/N3 PUFA interactions.
发展中国家肥胖症及腹型肥胖率的增长归因于饮食转变，即从传统的富含纤维的饮食转向富含加工食品、糖和不健康脂肪的西式饮食。环境变化，如改善所摄入膳食脂肪的质量，可能有助于预防或减轻具有遗传易感性个体的肥胖或不健康肥胖表型，尽管这一点尚未得到证实。因此，在本研究中，我们调查了基于卡雷利斯标准的代谢健康肥胖（MHO）或代谢不健康肥胖（MUO）的膳食脂肪质量指数如何与伊朗成年女性的遗传易感性相互作用。
在当前的横断面研究中，279名超重或肥胖女性参与其中。使用147项食物频率问卷评估膳食摄入量，并使用胆固醇饱和脂肪指数（CSI）和ω-6/ω-3（N6/N3）必需脂肪酸比值评估膳食脂肪质量。通过聚合酶链反应-限制性片段长度多态性（PCR-RFLP）技术对三个单核苷酸多态性——MC4R（rs17782313）、CAV-1（rs3807992）和Cry-1（rs2287161）进行基因分型，并将其合并以产生遗传风险评分（GRS）。使用多频生物电阻抗分析仪评估身体成分。根据卡雷利斯标准进行代谢风险评估后，将参与者分为MHO或MUO表型。
在控制混杂因素（年龄、体重指数、能量和身体活动）的调整模型中，我们发现GRS与N6/N3之间存在显著相互作用（β = 2.26，95%置信区间：0.008至4.52，P = 0.049）。此外，在MUH肥胖表型的原始模型（β = 1.92，95%置信区间：-0.06至3.91，P = 0.058）和调整模型（年龄和能量）（β = 2.00，95%置信区间：-0.05至4.05，P = 0.057）中，我们发现GRS与N6/N3之间存在边缘显著相互作用。然而，在原始模型和调整模型中，GRS与CSI之间均未显示出显著相互作用。
本研究强调了个性化营养的重要性，并建议根据基因-N6/N3多不饱和脂肪酸相互作用的研究结果，进一步研究广泛不同的脂肪摄入量。
