Masip Guiomar, Han Hannah Yang, Meng Tongzhu, Nielsen Daiva E
School of Human Nutrition, McGill University, Montreal, Quebec, Canada.
Growth, Exercise, Nutrition and Development (GENUD), Research Group, Instituto Agroalimentario de Aragón (IA2), Instituto de Investigación Sanitaria Aragón (IIS Aragón) Universidad de Zaragoza, Zaragoza, Spain.
Obes Rev. 2025 Sep;26(9):e13941. doi: 10.1111/obr.13941. Epub 2025 May 16.
Diet is an important determinant of body weight and may modulate genetic susceptibility to obesity.
This systematic review and meta-analysis aimed to synthesize evidence related to interactions between polygenic risk and nutrient intakes on obesity outcomes.
MEDLINE, EMBASE, Web of Science, and Cochrane Library were systematically searched to identify observational studies that assessed interactions between polygenic risk and nutrient intakes on obesity-related outcomes. Random effects meta-analyses were performed for pooled polygenic risk score (PRS)-total fat intake and PRS-protein intake interaction coefficients on body mass index (BMI).
Twenty-six publications were retrieved with studies conducted among European, Asian, and African samples. Dietary fats (saturated fat, omega-3, and trans fat) and energy intake were most frequently reported to interact with PRS on obesity outcomes, but the total number of studies available was low. No significant interactions were identified in meta-analyses of PRS interactions with total fat intake and protein intake on BMI. Several studies were rated as low quality, heterogeneity was high, and although study samples were racially diverse, PRSs tended to be based on samples of European ancestry.
Evidence of interactions between polygenic risk and nutrient intakes on obesity outcomes is limited and inconsistent. Further research addressing limitations related to study quality and polygenic risk characterization is needed.
饮食是体重的重要决定因素,可能调节肥胖的遗传易感性。
本系统评价和荟萃分析旨在综合多基因风险与营养素摄入量之间相互作用对肥胖结局影响的证据。
系统检索MEDLINE、EMBASE、科学网和考克兰图书馆,以识别评估多基因风险与营养素摄入量之间相互作用对肥胖相关结局影响的观察性研究。对体重指数(BMI)的汇总多基因风险评分(PRS)-总脂肪摄入量和PRS-蛋白质摄入量相互作用系数进行随机效应荟萃分析。
检索到26篇出版物,研究对象包括欧洲、亚洲和非洲样本。饮食脂肪(饱和脂肪、ω-3脂肪酸和反式脂肪)和能量摄入与PRS在肥胖结局方面的相互作用报道最为频繁,但现有研究总数较少。在PRS与总脂肪摄入量和蛋白质摄入量对BMI的相互作用的荟萃分析中未发现显著相互作用。几项研究质量评级较低,异质性较高,尽管研究样本种族多样,但PRS往往基于欧洲血统的样本。
多基因风险与营养素摄入量之间相互作用对肥胖结局影响的证据有限且不一致。需要进一步研究解决与研究质量和多基因风险特征相关的局限性。