Influence of Apolipoprotein A-I and B Genetic Variations on Insulin Resistance and Metabolic Syndrome in Obstructive Sleep Apnea

2019 ◽  
Author(s):  
Xinyi Li ◽  
Yuenan Liu ◽  
Huajun Xu ◽  
Yingjun Qian ◽  
Jianyin Zou ◽  
...  
CHEST Journal ◽  
2010 ◽  
Vol 138 (4) ◽  
pp. 615A
Author(s):  
Hwa Sik Moon ◽  
Hyeon Hui Kang ◽  
Sang Haak Lee ◽  
Jin Woo Kim ◽  
Chan Kwon Park ◽  
...  

2020 ◽  
Author(s):  
Li Xinyi ◽  
Fu Zhihui ◽  
Xu Huajun ◽  
Zou Jianyin ◽  
Zhu Huaming ◽  
...  

Abstract 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 5,259 subjects were examined. After strict screening, four APOA-I SNPs and five APOB SNPs in 4,007 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 Patients with insulin resistance had a lower APOA-I GRS and higher APOB levels after adjustments [odds ratio (OR) = 0.917, P = 0.001; OR = 3.168, P < 0.001, respectively]. Individuals with MetS had a lower APOA-I GRS and higher APOB levels after adjustments (OR = 0.870, 6.098, respectively, all P < 0.001). 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 MetS.


2006 ◽  
Vol 11 (1) ◽  
pp. 23-30 ◽  
Author(s):  
Altan Onat ◽  
Gülay Hergenç ◽  
Hüseyin Uyarel ◽  
Mehmet Yazıcı ◽  
Mustafa Tuncer ◽  
...  

2020 ◽  
Author(s):  
Li Xinyi ◽  
Fu Zhihui ◽  
Xu Huajun ◽  
Zou Jianyin ◽  
Zhu Huaming ◽  
...  

Abstract 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 5,259 subjects were examined. After strict screening, four APOA-I SNPs and five APOB SNPs in 4,007 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.


2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Xinyi Li ◽  
Zhihui Fu ◽  
Huajun Xu ◽  
Jianyin Zou ◽  
Huaming Zhu ◽  
...  

Abstract 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.


2019 ◽  
pp. 27-39
Author(s):  
O. O. Tolstikova ◽  
S. F. Aharkov

Metabolic syndrome (MS) is a growing serious health risk in adults, children and adolescents. The prevalence of metabolic syndrome ranges from 6 to 39 % depending on the criteria used. Multiple data have shown that MS is associated with a 2-fold increase in cardiovascular disorders and a 1.5-fold increase in all cause mortality. To date, there is no single definition regarding MS for children and adolescents. However, most authors agree with the components needed to diagnose such as central obesity, impaired glucose tolerance (or diabetes), hypertension, and dyslipidemia; each of which presents a serious risk of cardiovascular disease. Overweight and obesity are often seen in children and adolescents in the developed and developing countries with a prevalence of 20–35 %. A number of authors have emphasized the need for a modern adapted definition of MS in children and adolescents. For this purpose, it is necessary to take into account age and sex-dependent anthropometric, metabolic and cardiovascular parameters. Recently, a link has been established between metabolic syndrome and non-alcoholic fatty liver disease, as well as hyperuricemia and sleep disorders. According to current data, NAFLD and MS are closely related, so NAFLD is described as a manifestation of MS in the liver, with insulin resistance being the driving force of pathogenesis. A recent study found that 66 % of children with NAFLD confirmed by biopsy had MS, 63 % had hypertriglyceridemia, 45 % had low HDL cholesterol, 40 % had hypertension, and 10 % had impaired glucose tolerance. The correlation between levels of serum uric acid, MS and some of its components in children and adolescents is described. Hyperuricemia triggers endothelial dysfunction via vasodilation caused by insulin action. Obstructive sleep apnea is associated with MS in children and adolescents and is described as one of the components of MS. In 59 % of children with obstructive sleep apnea, signs of metabolic syndrome are noted. Biomarkers, such as adipocytokines, have been the subject of current research as they are implicated in the pathogenesis of MS. Recently, several adipocytokines and inflammatory cytokines have been identified that have significant positive (leptin, hemerin, vaspine, TNFα, IL-6, and IL-8) or Negative (adiponectin) associations with metabolic risk factors. Some may be considered pathophysiological factors that link obesity and its complications, such as insulin resistance and NAFLD. Epigenetics and gestational programming are important issues in addressing MS in children and adolescents. The role of micro-RNA in the diagnosis, stratification and therapy of MS is increasing. Early identification of risk factors, screening for metabolic disorders and the identification of new treatments are the primary goals of reducing morbidity and mortality. Currently, officially accepted approaches to treating children and adolescents with MS are dietary changes and physical activity. Pharmacological therapy and the use of bariatric (metabolic) surgery is a topic of discussion and is recommended for adolescents in some cases of high-risk MS.


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