Influence of multiple apolipoprotein A-I and B genetic variations on insulin resistance and metabolic syndrome in obstructive sleep apnea.
Influence of multiple apolipoprotein A-I and B genetic variations on insulin resistance and metabolic syndrome in obstructive sleep apnea.
复制标题
多种载脂蛋白 A-I 和 B 遗传变异对阻塞性睡眠呼吸暂停患者胰岛素抵抗和代谢综合征的影响
DOI：
10.1186/s12986-020-00501-8
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发表时间：
2020
影响因子：
4.5
通讯作者：
Yin S
中科院分区：
文献类型：
--
作者：
Li X;Fu Z;Xu H;Zou J;Zhu H;Li Z;Su K;Huai D;Yi H;Guan J;Yin S
背景
OSA 中载脂蛋白 A-I (APOA-I)、载脂蛋白 B (APOB) 与胰岛素抵抗、代谢综合征 (MetS) 之间的关系尚不清楚。我们的目的是评估 APOA-I 和 APOB 的多个单核苷酸多态性 (SNP) 变体是否对 OSA 中的胰岛素抵抗和 MetS 发挥协同作用。
方法
最初，对 5259 名受试者的 12 个 APOA-I SNP 和 30 个 APOB SNP 进行了检查。经过严格筛选，4007名参与者中的4个APOA-I SNP和5个APOB SNP被纳入。对于每个参与者，遗传风险评分（GRS）是根据 APOA-I 和 APOB 的多个遗传变异的累积效应计算的。 Logistic回归分析用于评估APOA-I/APOB基因多态性、胰岛素抵抗和OSA中MetS之间的关系。
结果
根据年龄、性别和 BMI 进行调整后，血清 APOB 水平增加了胰岛素抵抗和 MetS 的风险 [比值比（分别为 OR = 3.168，P < 0.001；OR = 6.098，P < 0.001]）。调整后，APOA-I GRS 降低了胰岛素抵抗和 MetS 的风险（OR = 0.917，P = 0.001；OR = 0.870，P） APOB GRS 与胰岛素抵抗没有关联（OR = 1.364，P = 0.610），并且在调整后与 MetS 关联较弱（OR = 1.072，P = 0.042）。此外，APOA-I 遗传评分分布前五分位的个体在调整后具有较低的胰岛素抵抗和 MetS 风险（OR = 0.761，P = 0.042）。 0.007；OR = 0.637，P 0.001）。
结论
在 OSA 患者中，APOA-I 遗传变异的累积效应降低了胰岛素抵抗和 MetS 的风险，而多个 APOB 遗传变异与胰岛素抵抗没有关联，与 MetS 的关联较弱。
Background
The relationships between apolipoprotein A-I (APOA-I), apolipoprotein B (APOB) with insulin resistance, metabolic syndrome (MetS) are unclear in OSA. We aimed to evaluate whether the multiple single nucleotide polymorphism (SNP) variants of APOA-I and APOB exert a collaborative effect on insulin resistance and MetS in OSA.
Methods
Initially, 12 APOA-I SNPs and 30 APOB SNPs in 5259 subjects were examined. After strict screening, four APOA-I SNPs and five APOB SNPs in 4007 participants were included. For each participant, the genetic risk score (GRS) was calculated based on the cumulative effect of multiple genetic variants of APOA-I and APOB. Logistic regression analyses were used to evaluate the relationships between APOA-I/APOB genetic polymorphisms, insulin resistance, and MetS in OSA.
Results
Serum APOB levels increased the risk of insulin resistance and MetS adjusting for age, gender and BMI [odds ratio (OR = 3.168, P 0.001; OR = 6.098, P 0.001, respectively]. APOA-I GRS decreased the risk of insulin resistance and MetS after adjustments (OR = 0.917, P = 0.001; OR = 0.870, P 0.001, respectively). APOB GRS had no association with insulin resistance (OR = 1.364, P = 0.610), and had weak association with MetS after adjustments (OR = 1.072, P = 0.042). In addition, individuals in the top quintile of the APOA-I genetic score distribution had a lower risk of insulin resistance and MetS after adjustments (OR = 0.761, P = 0.007; OR = 0.637, P 0.001, respectively).
Conclusions
In patients with OSA, cumulative effects of APOA-I genetic variations decreased the risk of insulin resistance and MetS, whereas multiple APOB genetic variations had no associations with insulin resistance and weak association with MetS.
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