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宏量营养素摄入调节 ApoB 基因 EcoRI 多态性对 2 型糖尿病患者血脂谱和炎症标志物的影响。

Macronutrient intake modulates impact of EcoRI polymorphism of ApoB gene on lipid profile and inflammatory markers in patients with type 2 diabetes.

机构信息

Department of Community Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences, Tehran, Iran.

Department of Cellular and Molecular Nutrition, School of Nutritional Sciences and Dietetics, Tehran University of Medical Sciences (TUMS), Tehran, PO Box: 141556117, Iran.

出版信息

Sci Rep. 2022 Jun 22;12(1):10504. doi: 10.1038/s41598-022-13330-x.

DOI:10.1038/s41598-022-13330-x
PMID:35732646
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9217912/
Abstract

We sought to examine whether dietary intakes may affect the relationship between ApoB EcoRI and lipid profile, as well as serum inflammatory markers, in patients with type 2 diabetes (T2DM). This current study consisted of 648 diabetic patients. Dietary intake was calculated by a food frequency questionnaire. Biochemical markers (high-density lipoprotein (HDL), total cholesterol (TC), LDL, TG, CRP, IL-18, PGF2α) were measured based on standard protocols. Genotyping of the Apo-B polymorphisms (rs1042031) was conducted by the PCR-RFLP method. The gene-diet interactions were evaluated using GLMs. In comparison to GG homozygotes, A-allele carriers with above the median -CHO intake (≥ 54 percent of total energy) had considerably greater TC and PGF2a concentrations. Furthermore, as compared to GG homozygotes, A-allele carriers with above the median protein intake (≥ 14 percent of total energy) had higher serum levels of TG (P = 0.001), CRP (P = 0.02), TG/HDL (P = 0.005), and LDL/HDL (P = 0.04) ratios. Moreover, A-allele carriers with above the median total fat intake (≥ 35 percent of total calories) had significantly higher TC level (P = 0.04) and LDL/HDL (P = 0.04) ratios compared to GG homozygotes. Furthermore, when compared to GG homozygotes, A-allele carriers who consumed above the median cholesterol (> 196 mg) had greater TG (P = 0.04), TG/HDL (P = 0.01) ratio, and IL-18 (P = 0.02). Furthermore, diabetic patients with the GA, AA genotype who consume above the median cholesterol had lower ghrelin levels (P = 0.01). In terms of LDL/HDL ratio, ApoB EcoRI and dietary intakes of specific fatty acids (≥ 9 percent for SFA and ≥ 12 percent for MUFA) had significant interaction. LDL/HDL ratio is greater in A-allele carriers with above the median SFA intake (P = 0.04), also when they consumed above the median MUFA this association was inverse (P = 0.04). Our study showed that plasma lipid levels in participants carrying the (AA or AG) genotype were found to be more responsive to increasing the percentage of energy derived from dietary fat, CHO, protein, SFA, and cholesterol consumption. Therefore, patients with a higher genetic susceptibility (AA or AG) seemed to have greater metabolic markers with a higher percentage of macronutrient consumption. Also, ApoB EcoRI correlations with metabolic markers might be attenuated with above the median MUFA consumption.

摘要

我们旨在研究饮食摄入是否会影响载脂蛋白 B EcoRI 与血脂谱以及血清炎症标志物之间的关系,这些研究对象为 2 型糖尿病(T2DM)患者。本研究共纳入了 648 名糖尿病患者。饮食摄入量通过食物频率问卷进行计算。根据标准方案测量生化标志物(高密度脂蛋白(HDL)、总胆固醇(TC)、LDL、TG、CRP、IL-18、PGF2α)。采用 PCR-RFLP 法对载脂蛋白 B 多态性(rs1042031)进行基因分型。采用 GLMs 评估基因-饮食相互作用。与 GG 纯合子相比,CHO 摄入量高于中位数(≥54%总能量)的 A 等位基因携带者 TC 和 PGF2a 浓度明显更高。此外,与 GG 纯合子相比,蛋白质摄入量高于中位数(≥14%总能量)的 A 等位基因携带者血清 TG(P=0.001)、CRP(P=0.02)、TG/HDL(P=0.005)和 LDL/HDL(P=0.04)比值更高。此外,与 GG 纯合子相比,总脂肪摄入量高于中位数(≥35%总热量)的 A 等位基因携带者 TC 水平(P=0.04)和 LDL/HDL(P=0.04)比值明显更高。此外,与 GG 纯合子相比,胆固醇摄入量高于中位数(>196mg)的 A 等位基因携带者 TG(P=0.04)、TG/HDL(P=0.01)比值和 IL-18(P=0.02)更高。此外,摄入胆固醇高于中位数的 GA、AA 基因型的糖尿病患者 ghrelin 水平更低(P=0.01)。就 LDL/HDL 比值而言,ApoB EcoRI 和特定脂肪酸(SFA≥9%和 MUFA≥12%)的饮食摄入量存在显著的相互作用。SFA 摄入量高于中位数的 A 等位基因携带者 LDL/HDL 比值更高(P=0.04),而 MUFA 摄入量高于中位数时,这种关联呈负相关(P=0.04)。我们的研究表明,携带(AA 或 AG)基因型的参与者的血浆脂质水平似乎更容易受到饮食中脂肪、CHO、蛋白质、SFA 和胆固醇消耗百分比增加的影响。因此,具有较高遗传易感性(AA 或 AG)的患者似乎具有更高的代谢标志物,其宏量营养素消耗的百分比更高。此外,ApoB EcoRI 与代谢标志物的相关性可能会随着 MUFA 摄入量高于中位数而减弱。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d46/9217912/841008739fe8/41598_2022_13330_Fig1a_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d46/9217912/841008739fe8/41598_2022_13330_Fig1a_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d46/9217912/841008739fe8/41598_2022_13330_Fig1a_HTML.jpg

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