Gene-diet interactions between CETP, LPL, and LIPC genetic risk score and dietary fat and carbohydrate intake on lipid levels in Mexican adults

IF 0.3 Q4 NUTRITION & DIETETICS

CAHIERS DE NUTRITION ET DE DIETETIQUE Pub Date : 2026-08-01 Epub Date: 2026-09-24 DOI:10.1016/j.cnd.2026.08.048

Zamudio-Felix Itzel, Andrade-Espinoza Mariana, Bojórquez-Iribe Aricel, González-Becerra Karina

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Dietary intake and fasting biochemical parameters were assessed using standardized procedures. Genotyping of CETP (rs708272), LPL (rs13702), and LIPC (rs1800588) was performed using TaqMan real-time PCR assays. Participants were classified according to an unweighted genetic risk score (uGRS) and grouped by the number of risk alleles. Linear regression models, analysis of covariance, and moderation analyses were used to examine gene–diet interactions between dietary fat and carbohydrate intake and lipid related metabolic outcomes. Approval was obtained from the Ethics (CEI-01-2025-08) and Biosafety (CBIO-01-2025-08) Committee of the University Center of Altos of the University of Guadalajara (CUALTOS-UdeG, Mexico).</div></div><div>A cross-sectional study was conducted among adults from western Mexico recruited between June 2024 and May 2026. Dietary intake and fasting biochemical parameters were assessed using standardized procedures. 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Furthermore, participants carrying 4–6 risk alleles and consuming>8% of total energy from polyunsaturated fatty acids (PUFAs) presented lower HDL-c concentrations (24.00mg/dL) than those consuming<8% of total energy from PUFAs (56.64mg/dL; <em>P</em>    =0.036).</div><div><h3>Conclusion</h3><div>The genetic risk by CETP, LPL, and LIPC variants may modulate the relationship between dietary fat and carbohydrate intake and lipid-related levels. The observed interactions suggest that individuals with different genetic profiles may exhibit distinct metabolic responses to dietary macronutrient intake, particularly regarding total cholesterol, triglyceride, and HDLc concentrations. 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引用次数: 0

Abstract

Objective

To evaluate the interaction between dietary lipid and carbohydrate intake and a combined genetic risk score (uGRS) based on CETP, LPL, and LIPC variants in relation to HDLc, triglyceride, and total cholesterol concentrations in Mexican adults.

Methods

A cross-sectional study was conducted among adults from western Mexico recruited between June 2024 and May 2026. Dietary intake and fasting biochemical parameters were assessed using standardized procedures. Genotyping of CETP (rs708272), LPL (rs13702), and LIPC (rs1800588) was performed using TaqMan real-time PCR assays. Participants were classified according to an unweighted genetic risk score (uGRS) and grouped by the number of risk alleles. Linear regression models, analysis of covariance, and moderation analyses were used to examine gene–diet interactions between dietary fat and carbohydrate intake and lipid related metabolic outcomes. Approval was obtained from the Ethics (CEI-01-2025-08) and Biosafety (CBIO-01-2025-08) Committee of the University Center of Altos of the University of Guadalajara (CUALTOS-UdeG, Mexico).

Results

A total 234 individuals were included in the analysis; significant gene–diet interactions were observed between the combined genetic risk score and dietary macronutrient intake. Participants with higher genetic risk (4–6 risk alleles) who consumed < 30% of total energy from lipids exhibited higher total cholesterol concentrations (230.57 mg/dL) than those consuming > 30% of total energy from lipids (150.54 mg/dL; P = 0.045). Furthermore, participants carrying 4–6 risk alleles and consuming > 8% of total energy from polyunsaturated fatty acids (PUFAs) presented lower HDL-c concentrations (24.00 mg/dL) than those consuming < 8% of total energy from PUFAs (56.64 mg/dL; P = 0.044). In addition, participants with a lower genetic risk (0–2 risk alleles) and a higher carbohydrate intake showed lower triglyceride concentrations (89.36 mg/dL) compared with those with a moderate genetic risk (3–4 risk alleles) and a higher carbohydrate intake (130.06 mg/dL; P = 0.036).

Conclusion

The genetic risk by CETP, LPL, and LIPC variants may modulate the relationship between dietary fat and carbohydrate intake and lipid-related levels. The observed interactions suggest that individuals with different genetic profiles may exhibit distinct metabolic responses to dietary macronutrient intake, particularly regarding total cholesterol, triglyceride, and HDLc concentrations. In this context, the combination of these variants may help identify dietary patterns that are more favorable to specific genetic profiles, thereby supporting the development of nutrigenetic recommendations to improve lipid metabolism.

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墨西哥成年人CETP、LPL和LIPC遗传风险评分与饮食脂肪和碳水化合物摄入对血脂水平的影响之间的基因-饮食相互作用

目的评估膳食脂质和碳水化合物摄入量与基于CETP、LPL和LIPC变异的与HDLc、甘油三酯和总胆固醇浓度相关的综合遗传风险评分（uGRS）之间的相互作用。评估膳食脂质和碳水化合物摄入量与基于CETP、LPL和LIPC变异的与HDLc、甘油三酯和总胆固醇浓度相关的综合遗传风险评分（uGRS）之间的相互作用。方法对2024年6月至2026年5月在墨西哥西部招募的成年人进行横断面研究。采用标准化程序评估膳食摄入量和空腹生化参数。采用TaqMan实时PCR技术对CETP （rs708272）、LPL （rs13702）和LIPC （rs1800588）进行基因分型。参与者根据未加权遗传风险评分（uGRS）进行分类，并根据风险等位基因的数量进行分组。使用线性回归模型、协方差分析和调节分析来检验膳食脂肪和碳水化合物摄入量与脂质相关代谢结果之间的基因-饮食相互作用。已获得瓜达拉哈拉大学（CUALTOS-UdeG，墨西哥）阿尔托斯大学中心伦理委员会（CEI-01-2025-08）和生物安全委员会（CBIO-01-2025-08）批准。一项横断面研究在2024年6月至2026年5月期间从墨西哥西部招募的成年人中进行。采用标准化程序评估膳食摄入量和空腹生化参数。采用TaqMan实时PCR技术对CETP （rs708272）、LPL （rs13702）和LIPC （rs1800588）进行基因分型。参与者根据未加权遗传风险评分（uGRS）进行分类，并根据风险等位基因的数量进行分组。使用线性回归模型、协方差分析和调节分析来检验膳食脂肪和碳水化合物摄入量与脂质相关代谢结果之间的基因-饮食相互作用。已获得瓜达拉哈拉大学（CUALTOS-UdeG，墨西哥）阿尔托斯大学中心伦理委员会（CEI-01-2025-08）和生物安全委员会（CBIO-01-2025-08）批准。结果共纳入234例；综合遗传风险评分与膳食宏量营养素摄入量之间存在显著的基因-饮食相互作用。具有较高遗传风险的参与者（4-6个风险等位基因）消耗30%总能量的脂质比消耗30%总能量的脂质（150.54 mg/dL, P = 0.045）表现出更高的总胆固醇浓度（230.57 mg/dL）。此外，携带4-6个风险等位基因并消耗多不饱和脂肪酸（PUFAs）总能量的8%的参与者的HDL-c浓度（24.00 mg/dL）低于消耗PUFAs总能量的8%的参与者（56.64 mg/dL, P = 0.044）。此外，较低遗传风险（0-2个风险等位基因）和较高碳水化合物摄入量的参与者与中等遗传风险（3-4个风险等位基因）和较高碳水化合物摄入量（130.06 mg/dL; P = 0.036）的参与者相比，甘油三酯浓度（89.36 mg/dL）较低。共有234人被纳入分析；综合遗传风险评分与膳食宏量营养素摄入量之间存在显著的基因-饮食相互作用。具有较高遗传风险的参与者（4-6个风险等位基因）消耗30%总能量的脂质比消耗30%总能量的脂质（150.54 mg/dL, P = 0.045）表现出更高的总胆固醇浓度（230.57 mg/dL）。此外，携带4-6个风险等位基因并消耗多不饱和脂肪酸（PUFAs）总能量的8%的参与者的HDL-c浓度（24.00 mg/dL）低于消耗PUFAs总能量的8%的参与者（56.64 mg/dL, P = 0.044）。此外，较低遗传风险（0-2个风险等位基因）和较高碳水化合物摄入量的参与者与中等遗传风险（3-4个风险等位基因）和较高碳水化合物摄入量（130.06 mg/dL; P = 0.036）的参与者相比，甘油三酯浓度（89.36 mg/dL）较低。结论CETP、LPL和LIPC变异的遗传风险可能调节膳食脂肪和碳水化合物摄入量与脂相关水平的关系。观察到的相互作用表明，具有不同遗传谱的个体可能对饮食宏量营养素摄入表现出不同的代谢反应，特别是在总胆固醇、甘油三酯和HDLc浓度方面。在这种情况下，这些变异的组合可能有助于确定更有利于特定遗传谱的饮食模式，从而支持营养遗传学建议的发展，以改善脂质代谢。CETP、LPL和LIPC变异的遗传风险可能调节膳食脂肪和碳水化合物摄入量与脂质相关水平之间的关系。观察到的相互作用表明，具有不同遗传谱的个体可能对饮食宏量营养素摄入表现出不同的代谢反应，特别是在总胆固醇、甘油三酯和HDLc浓度方面。在这种情况下，这些变异的组合可能有助于确定更有利于特定遗传谱的饮食模式，从而支持营养遗传学建议的发展，以改善脂质代谢。

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来源期刊

CAHIERS DE NUTRITION ET DE DIETETIQUE NUTRITION & DIETETICS-

CiteScore

0.60

自引率

33.30%

发文量

审稿时长

65 days

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