血管紧张素系统基因多态性与阻塞性睡眠呼吸暂停低通气综合征

目的 探讨血管紧张素转换酶(ACE)和血管紧张素原(AGT)基因与阻塞性睡眠呼吸暂停低通气综合征(OSAHS)发病的关系。方法 应用聚合酶链反应(PCR)和限制性长度多态性方法测定无亲缘关系的中国北方汉族男性121例OSAHS患者与100例非OSAHS对照者的ACE和AGT基因多态性的基因型,并检验两组基因型的分布、等位基因频率的差异和基因多态性对OSAHS患者组肥胖表型的效应,分析基因型与睡眠呼吸暂停低通气指数(AHI)、收缩压(SBP)与舒张压(DBP)的关系。结果 ACE基因多态性的基因型分布两组差异无显著性(P>0.05),OSAHS患者组AGT基因多态性的基因型分布和等位基因频率与对照组相比,差异有显著性(P<0.05),OSAHS患者组中AGT基因多态性T等位基因携带者的体重指数(BMI)、颈围(NC)、腰臀比(WHR)明显高于非携带者,AHI、SBP与DBP也相应明显高于非携带者,差异有显著性(P<0.05)。结论 ACE I/D基因多态性可能不参与中国北方汉族男性中心型肥胖及OSAHS的形成。AGT基因多态性可能通过中心型肥胖而导致中国北方汉族男性OSAHS的发生及OSAHS患者高血压的形成。     

阻塞性睡眠呼吸暂停低通气综合征与5-羟色胺2A受体A1438G基因多态性相关

目的 探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)发生与5-羟色胺(5-HT)2A受体A1438G基因多态性的相关性.方法 采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)方法,对无亲缘关系的汉族76例OSAHS患者及54名正常对照者5-HT 2A受体A1438G位点的基因多态性进行检测,比较两组基因型分布及等位基因频率的差异,分析基因型对OSAHS患者多导睡眠图(PSG)参数及肥胖指标的影响.结果 ①OSAHS组5-HT 2A受体A1438G位点的AA基因型及A等位基因频率显著高于对照组(2=17.139,P=0.002;2=27.785,P=0.001).②AA型比AG、GG型病情更重,但肥胖相关指标差异却无统计学意义(P均＞0.05).③与AG、GG型比较,AA型患者一级亲属中OSAHS的发病率更高(分别为24.5%、12.3%、34.7%).结论 5-HT 2A受体A1438G基因多态性与汉族OSAHS的发病可能有关,A等位基因可能是一易感基因,但它可能并不是通过中心性肥胖、颈部脂肪增加的途径导致OSAHS的发生.     

血管紧张素Ⅱ—1型受体（AT1R）基因多态性与OSAHS及OSAHS合并高血压的相关性

目的 探讨血管紧张素Ⅱ-1型受体(ATlR)基因A1166/C多态性与阻塞性睡眠呼吸暂停低通气综合征(OSAHS)及其合并高血压的相关性.方法 采用聚合酶链反应(PCR)、限制性内切酶酶切及电泳分型方法对OSAHS患者和正常对照人群的AT1R基因A1166/C位点的多态性进行观察,并结合多导睡眠监测结果进行分析.结果 正常人群及OSAHS患者的AT1R基因AA、AC、cC型的分布频率分别为88.2%、10.3%、1.5%和72.3%、26.3%、1.4%,两组构成差异有统计学意义(P<0.05).单纯OSAHS患者及OSAHS合并高血压患者等位基因A和C的频率分别为62%、38%和80%、20%差异显著(P<0.05).AC及CC基因型的OSAHS患者睡眠呼吸暂停低通气指数(AHI)、平均呼吸暂停时间,最低血氧饱和度均与从基因型患者差异有统计学意义(P<0.05).结论 OSAHS的发病与ATlR基因A/C多态性相关联,基因型AC和等位基因C可能是OSAHS发病的危险因素.     

中国北方汉族人2型糖尿病合并冠心病与KIF6基因Trp719Arg多态性的相关性

目的探讨中国北方汉族人群KIF6基因Trp719Arg多态性基因型和等位基因频率分布特点,及与2型糖尿病(DM)合并冠心病(CHD)的关联性。方法采用病例对照研究设计,应用聚合酶链反应限制性片段长度多态性(PCR-RFLP)技术分析了对照组(152例)、DM组(97例)、DM+CHD组(76例)KIF6基因Trp719Arg多态性;比较组间基因型和等位基因频率分布差异,研究基因多态性对血糖、血脂水平的影响。结果中国北方汉族人群Trp719Arg多态性TT、TC、CC基因型频率分别为0.281、0.499与0.220。T、C等位基因频率分别为0.531与0.469。KIF6基因Trp719Arg多态性基因型和等位基因频率组间分布差异无统计学意义(均为P>0.05)。KIF6基因Trp719Arg多态性对血糖、血脂水平无显著影响。Logistic回归分析显示,高血压、年龄(≥60岁)、低HDL-C水平(<1.04 mmol/L)是DM+CHD的独立危险因素(OR分别为2.850、12.977和4.006,均为P<0.05),C等位基因与DM+CHD的发生无统计学相关性。结论 KIF6基因Trp719Arg多态性可能不是我国北方汉族人群DM+CHD的独立危险因素。     

阻塞性睡眠呼吸暂停低通气综合征患者载脂蛋白E基因多态性分析

目的 探讨载脂蛋白E(apoliporotein E,ApoE)基因多态性与阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea hyopnea syndrome,OSAHS)之间的关系.方法 选取经多导睡眠仪确诊的84例无亲缘关系的OSAHS患者(OSAHS组)和排除OSAHS的106位正常人群(正常对照组),采用聚合酶链反应限制性片段长度多态性方法,检测两组ApoE基因多态性的基因型,同时检测两组血清甘油三脂(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇(LDL-C)水平和体质量指数,分析基因型分布、等位基因频率差异、不同等位基因与OSAHS患者血脂水平的关系.结果 OSAHS组ApoEε4等位基因频率明显高于正常对照组,差异有统计学意义(P＜0.01);携带ApoEε4等位基因的OSAHS组患者睡眠呼吸暂停指数高于携带ApoEε3等位基因的OSAHS组患者,差异有统计学意义(P＜0.01);携带ApoEε4等位基因的OSAHS组患者TC水平高于携带ApoEε2和ApoEε3组,差异有统计学意义(P＜0.01).OSAHS组患者TG、LDL-C高于正常对照组,差异有统计学意义(P＜0.05).结论 OSAHS发病与ApoE基因多态性相关联,ApoEε4等位基因町能是OSAHS发病的危险因素.OSAHS患者存在血脂代谢紊乱,携带ApoEε4等位基因的OSAHS患者血清胆固醇升高更明显.     

β1肾上腺素能受体Gly 389Arg多态性与原发性高血压的关系

目的:探讨汉族人群β1肾上腺素能受体Gly 389Arg多态性与原发性高血压的关系. 方法:采用聚合酶链反应-限制性长度片段多态性技术分析原发性高血压患者和正常人群β1肾上腺素能受体Gly 389Arg多态性.结果:高血压组Arg/Arg,Arg/Gly,Gly/Gly基因型频率分别为59.06%、35.09%、5.85%,正常对照组分别为43.55%、45.97%、10.48%;两组间三种基因型频率分布有统计学差异(x2=7.420,P＜0.05);高血压组Arg等位基因频率为76.61%,Gly等位基因频率为23.39%,正常对照组分别为66.53%、33.47%,两组间等位基因频率分布存在统计学差异(x2=7.299,P＜0.05);高血压组Arg纯合子基因型频率和Arg等位基因频率均明显高于对照组. 结论:β1肾上腺素能受体Gly 389Arg多态性可能与原发性高血压发病有关.     

阻塞性睡眠呼吸暂停低通气综合征患者肾上腺素β_1受体基因多态性与其心血管系统并发症的关系

目的 探讨OSAHS患者肾上腺素β_1受体基因多态性与其心血管系统并发症的相关性.方法 采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)技术对2007年2月至12月山西医科大学第二医院经多导睡眠监测(PSG)诊断的192例OSAHS患者肾上腺素β_1受体Gly389Arg位点的基因多态性进行检测,分析该位点基因型(CC组、CG组及GG组)与OSAHS患者PSG监测参数及心血管事件的相关性.采用方差分析,x~2检验及t检验进行统计学分析.结果 不同基因型频率两两比较CC组明显高于CG和GG组,等位基因频率C明显高于G.CC组的睡眠时最低血氧饱和度(minSaO_2)明显低于GG和CG组,睡眠期间SaO_2低于90%的时间占总睡眠时间的百分比(T90)及最长呼吸暂停时间(Tmax)均较高.3组间窦性心动过缓的发生率差异无统计学意义(P>0.05),CC组高血压、冠状动脉粥样硬化性心脏病、心律失常及肺源性心脏病的发生率均明显高于CG组和GG组(P<0.05).结论 OSAHS患者肾上腺素β_1受体Gly389Arg位点的CC基因型可能与其心血管并发症的发生有关,C等位基因可能是易感基因.     

瘦素基因2548G/A多态性与阻塞性睡眠呼吸暂停低通气综合征易感性的关系探讨

目的探讨瘦素基因2548G/A基因多态性与阻塞性睡眠呼吸暂停低通气综合征(OSAHS)易感性的关系。方法采用聚合酶链反应—限制性片段长度多态性(PCR-RFLP)方法检测90例肥胖OSAHS患者(A组)、93例非肥胖OSAHS患者(B组)、105例单纯肥胖者(B组)及96例健康人(D组)瘦素基因2548G/A的基因型并计算等位基因频率,分析其与OSAHS易感性的关系。结果各组基因型及等位基因比较均无统计学差异(P均>0.05);在OSAHS患者中,AA基因型患者腰臀比明显低于AG型和GG型(P均<0.05),余指标比较均无统计学差异(P均>0.05)。结论瘦素基因2548G/A多态性与OSAHS的发病无关,但2548G/A变异可能与腹型肥胖的发生有关。     

瘦素受体基因多态性与云南地区高血压合并肥胖的相关性

目的 探讨瘦素受体(LEPR)基因多态性与云南地区汉族人口高血压合并肥胖的相关性.方法 选取云南地区汉族高血压病住院患者283例,同期选取正常对照组153例.将高血压组以体质指数(BMI)≥28 kg/m2划分为肥胖高血压组162例和单纯高血压组121例两个亚组.运用聚合酶连反应限制性片段长度多态性(PCRRELP)方法测定LEPR基因Gln223Arg和Lys109Arg多态性.采用彩色超声诊断仪测定颈动脉内膜中膜厚度(CIMT).结果 LEPR基因Gln223Arg基因型频率和等位基因频率在高血压组和对照组之间分布有统计学意义(P＜0.01); LEPR基因Lys109Arg基因型频率和等位基因频率在高血压组和对照组之间分布无统计学意义(P＞0.05).LEPR基因Gln223Arg等位基因A的频率在肥胖高血压明显高于单纯高血压组(P＜0.01),并且有着更厚颈动脉内膜中膜厚度(P＜0.05).Lys109Arg基因型频率在肥胖高血压组临床资料比较中差异无统计学意义.结论 LEPR基因Gln223Arg与高血压合并肥胖明显相关;且A等位基因是高血压合并肥胖人群发生动脉粥样硬化的危险因素;Lys109Arg多态性与高血压及各项临床特征比较无明显相关.     

汉族人群5-羟色胺受体基因多态性与阻塞性睡眠呼吸暂停低通气综合征的相关性

目的 探讨5-羟色胺2A、2C受体基因多态性与阻塞性睡眠呼吸暂停低通气综合征(OSAHS)的相关性,寻找与OSAHS发生有关的基因型.方法 采用聚合酶链反应-限制性片段长度多态性方法,对65例OSAHS患者(OSAHS组)及54例健康对照组5-羟色胺2A受体T102C、A1438G和2C受体G796C位点的基因多态性进行检测,比较两组基因型分布及等位基因频率的差异,分析基因型与OSAHS患者多导睡眠图参数及肥胖指标的相关性.采用方差分析、Fisher检验、t检验、x2检验进行统计学分析.结果 两组5-羟色胺2A受体T102C和2C受体G796C位点的基因型分布及等位基因频率无明显差别;OSAHS组5-羟色胺2A受体T102C位点TT、TC、CC基因型和T、C等位基因频率与健康对照组无明显差别;OSAHS组5-羟色胺2C受体G796C位点男性G、C半合子型,女性GG、GC基因型和G、C等位基因频率与健康对照组无明显差别;OSAHS组5-羟色胺2A受体A1438G位点的AA基因型和A等位基因频率[63.1%(41/65)、74.6%(97/130)]明显高于健康对照组[27.8%(15/54)、40.7%(44/108)];OSAHS组AA型的阻塞性呼吸暂停低通气指数[(40±9)次/b]明显高于AG、GG型[(25±9)次/h、(20±11)次/h],AA型的最长呼吸暂停时间[(94±10)s]明显长于AG、GG型[(88±9)s、(75±12)s],AA型最低血氧饱和度[(69±12)%]明显低于AG、GG型[(78±10)%、(80±9)%],3种基因型的体重指数、颈围和腰臀比无明显差别.结论 5-羟色胺2A受体T102C和2C受体G796C位点的基因多态性可能与汉族人群OSAHS的发病无关,5-羟色胺2A受体A1438G位点的AA基因型可能与汉族人群OSAHS的发病有关,A等位基因可能是易感基因.     

Interactions among the alpha2-, beta2-, and beta3-adrenergic receptor genes and obesity-related phenotypes in the Quebec Family Study

The gene-gene interactions between markers in the alpha2-, beta2-, and beta3-adrenergic receptor (ADR) genes and obesity-related phenotypes were studied in the Quebec Family Study (QFS) cohort. The prevalence of the Arg allele of the Arg16Gly polymorphism in the beta2-ADR gene was higher (49%) in males with a body mass index (BMI) of 35 kg/m2 or higher versus those with a BMI less than 35 kg/m2 (33%; P = .010). The beta2-ADR gene Arg16Gly and Gln27Glu polymorphisms were associated with plasma total and low-density lipoprotein (LDL) cholesterol concentrations. In addition, the homozygotes for the 6.3-kb allele of DraI polymorphism in the alpha2-ADR gene had the lowest mean abdominal subcutaneous fat area (P = .012) and total fat area (P = .003), as well as insulin area, under the curve during an oral glucose tolerance test ([OGTT] P = .004). Several ADR gene-gene interaction effects on abdominal fat distribution and plasma lipids were detected. First, significant interactions between alpha2- and beta3-ADR genes were observed on total (P = .015) and subcutaneous (P = .004) abdominal fat. Second, interaction effects between alpha2- and beta2-ADR gene variants influenced total, high-density lipoprotein (HDL), and LDL cholesterol concentrations. Finally, there were interactions between markers within the beta2-ADR gene affecting plasma triglyceride concentrations and subcutaneous abdominal fat. From these results, we conclude that polymorphisms in the ADR genes contribute to body fat and plasma lipid variability in men. Gene-gene interactions among the ADR genes contribute to the phenotypic variability in abdominal obesity and plasma lipid and lipoprotein, but not in visceral fat levels.     

瘦素受体基因Gln223Arg多态性与阻塞性睡眠呼吸暂停低通气综合征的关系

目的　探讨瘦素受体 (Lepr)基因Gln2 2 3Arg多态性与阻塞性睡眠呼吸暂停低通气综合征 (OSAHS)之间的关系。方法　采用聚合酶链反应 限制性片段长度多态性 (PCR RFLP)方法 ,测定181例中国北方地区汉族人Gln2 2 3Arg多态性的基因型 (其中OSAHS组 10 3例 ,非OSAHS对照组 78例 ) ,同时测定体重指数 (BMI)、颈围 (NC)、腰臀比 (WHR)以及醒后血压 (Bp)、醒后心率 (HR)、多导睡眠图 (PSG)。其中OSAHS组 6 0例 ,非OSAHS对照组 4 0例进行了血清空腹血糖 (FBG)、甘油三酯 (TG)、胆固醇 (Chol)、空腹真胰岛素 (TI)及血清瘦素 (Lep)的测定。结果　携带瘦素受体GG基因型的OSAHS患者颈围明显较 (GA +AA)基因型颈围大 [(41 4 6± 0 34)cmvs (39 85± 0 70 )cm ,P =0 0 31];Gln2 2 3Arg多态性与北方地区汉族人OSAHS无显著相关性 (χ2 =0 783,P =0 6 76 ) ;Gln2 2 3Arg不同基因型与OSAHS的总体脂、Bp、Lep、TI、FBG、TG、Chol及PSG各参数间不存在相关性 (P >0 0 5 )。结论　Lepr基因Gln2 2 3Arg多态性可能参与了OSAHS颈部脂肪选择性分布的调节 ,但其在北方地区汉族OSAHS的发病中可能无重要作用 ;目前的研究未发现Gln2 2 3Arg的基因型与OSAHS的BMI、高血压、FBG、TI、Lep、TG、Chol水平以及PSG参数之间存在相关性。     

肿瘤坏死因子基因多态性与阻塞性睡眠呼吸暂停低通气综合征

目的探讨肿瘤坏死因子α(TNF-α)启动子上游308位点(TNF-αG-308A)多态性与阻塞性睡眠呼吸暂停低通气综合征(OSAHS)的关系。方法研究对象为2004年6月至2005年12月我院睡眠检测中心就诊的患者。采用酶联免疫吸附测定(ELISA)法测定76例 OSAHS 组和42例非OSAHS 对照组血清中 TNF-α水平,并对76例中的18例患者进行持续气道正压通气(CPAP)治疗,测定治疗1个月后患者血清中 TNF-α水平;采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)方法,检测76例患者 TNF-αG-308A 基因多态性频率及分布,分析该基因多态性与体重指数(BMI)、颈围、腰臀比、多导睡眠图监测(PSG)相关参数以及收缩压、舒张压等的关系。结果 OSAHS 组 TNF-α的血清水平[(12.32±3.62)ng/L]较对照组[(8.59±1.62)ng/L]明显增高(t=7.716,P<0.01);18例患者进行 CPAP 治疗1个月后血清中 TNF-α水平下降为(10.31±1.91)ng/L,但仍未恢复至正常水平;OSAHS 组 AA/AG 基因型频率(31/76,41%)显著高于对照组(7/42,17%;X~2=7.485,P<0.05),其 A 等位基因频率(39/152,25.7%)高于对照组(39/152,9.5%),差异有统计学意义(X~2=8.830,P<0.01)。OSAHS 组 AA/AG 基因型患者血清中 TNF-α水平、颈围、腰臀比、呼吸暂停低通气指数(AHI)[分别为(13.39±3.71)ng/L、(45.2±4.2)cm、(0.91±0.12)和(34.8±15.6)次/h]均高于 GG 基因型[分别为(11.09±3.54)ng/L、(42.7±4.9)cm、(0.85±0.12)和(26.4±12.3)次/h],而最低血氧饱和度(LSaO_2)前者低于后者[(78.8±10.9)%,(83.4±8.6)%],差异均有统计学意义(t 值分别为2.725,2.278,2.150,2.609,2.039;P<0.05或<0.01);BMI、收缩压、舒张压比较差异无统计学意义。结论 OSAHS 的发病与 TNF-αG-308A 基因多态性相关,该基因多态性可能在一定程度上增加了 OSAHS 的遗传易感性。     

不同严重度阻塞性睡眠呼吸暂停低通气综合征女性血压影响因素分析

目的:探讨不同严重度阻塞性睡眠呼吸暂停低通气综合征(OSAHS)女性患者血压的影响因素。方法:将190例2009至2011年就诊于上海交通大学医学院附属瑞金医院睡眠中心的女性打鼾患者按睡眠呼吸暂停低通气指数(AHI)分成4组:非OSAHS组、轻度OSAHS组、中度OSAHS组和重度OSAHS组,比较这4组患者的一般特征、多导睡眠图(PSG)监测指标及血压的差异,并分析不同OSAHS严重度组血压影响因素。结果:非OSAHS组43例,轻度OSAHS组52例,中度OSAHS组30例,重度OSAHS组65例。随着AHI升高,各组血压值呈升高趋势。各组血压比较,重度OSAHS组收缩压与非OSAHS组比较有显著差异(P<0.05);重度OSAHS组舒张压高于非OSAHS组及轻度OSAHS组(P     

The Arg64 allele of the beta 3-adrenoceptor gene but not the -3826G allele of the uncoupling protein 1 gene is associated with increased leptin levels in the Spanish population

To determine whether there are variations in leptin levels according to the beta(3)-adrenoceptor (beta(3)-AR) Trp64Arg and uncoupling protein 1 (UCP1) -3826A-->G polymorphisms, given the regulatory role of catecholamines through the beta(3)-AR in leptin production and the previously reported association of the UCP1 -3826A-->G variant with obesity. A total of 160 men and 172 women randomly chosen from a nationwide population-based obesity cross-sectional survey in Spain were studied. Body mass index (BMI), waist-to-hip ratio (WHR), leptin, insulin, fasting and 2-hour post-glucose load glycemia, high-density lipoprotein (HDL)-, low-density lipoprotein (LDL)-, and total cholesterol, and triglyceride plasma levels were measured. beta(3)-AR Trp64Arg and UCP1 -3826A-->G genotypes were determined by restriction fragment length polymorphism-polymerase chain reaction (RFLP-PCR). UCP1 -3826G allele frequency was higher in men than in women (0.31 v 0.22, P = .015) and in obese women than in non-obese women (0.31 v 0.17, P = .008). Women carriers of the Arg64 or the alleles also showed higher leptin levels than noncarriers. Multiple linear regression analysis showed that the Arg64 allele is associated with higher leptin levels after the adjustment for gender, age, WHR, and the degree of glucose tolerance. In conclusion, the beta(3)-AR Trp64Arg polymorphism might have an impact on the mechanisms involved in leptin release from adipose tissue. Furthermore, our results agree with the previously reported association between UCP1 -3826G allele and obesity and point to a gender-related effect.     

Association of Trp64Arg polymorphism of the beta3-adrenergic receptor gene and no association of Gln223Arg polymorphism of the leptin receptor gene in Japanese schoolchildren with obesity

OBJECTIVE: To investigate whether Trp64Arg polymorphism of the beta3-adrenergic receptor (beta3-AR) gene and Gln223Arg polymorphism of the leptin receptor (Ob-R) gene are associated with obesity in Japanese schoolchildren. DESIGN: Population study of participants from a rural town located within 50 km northeast of Tokyo based on school medical examinations. SUBJECTS: 553 Japanese schoolchildren (291 boys and 262 girls) who were 9-15 y old with a mean age of 11.9 +/- 1.8 y. MEASUREMENTS: DNA was extracted from whole blood and genotyped by PCR-RFLP. Height, weight and blood pressure were measured in school medical examinations. Total cholesterol, triglyceride and HDL-cholesterol concentrations were measured by an autoanalyzer. Obesity index, body mass index (BMI) and LDL-cholesterol concentration were calculated by the respective formulae. RESULTS: In Trp64Arg polymorphism of the beta3-AR gene, the number of obese subjects with Trp/Arg or Arg/Arg genotypes was significantly higher than that of the non-obese subjects (chi2=5.79, P=0.02). The obesity index of subjects with the Arg/Arg or Arg/Trp genotype was significantly higher than that of those with the Trp/Trp genotype (8.2 +/- 18.7% vs 4.5 +/- 15.8%, P=0.04). Moreover, after adjustments for age and gender, BMI of subjects with the Trp/Arg or Arg/Arg genotype was significantly higher than that of those with the Trp/Trp genotype (19.4 +/- 3.6 kg/m2 vs 18.9 +/- 3.2 kg/m2, P= 0.02). However, no significant differences were observed in the clinical characteristics among the genotype groups of the Ob-R gene. CONCLUSIONS: Trp64Arg polymorphism of the beta3-AR gene appears to be a genetic risk factor for obesity in Japanese children, but Gln223Arg polymorphism of the Ob-R gene does not appear to be associated with obesity.     

阻塞性睡眠呼吸暂停低通气综合征与胰岛素抵抗的关系

目的探讨阻塞性睡眠呼吸暂停低通气综合征（OSAHS）与胰岛素抵抗（IR）的关系。方法选男性肥胖OSAHS患者60例（肥胖OSAHS组）、非OSAHS肥胖男性60例（肥胖非OSAHS组）、体重正常非OSAHS男性60例（正常体重非OSAHS组）,计算3组受试者的腰臀比和体重指数（BMI）;观察脉搏血氧饱和度（SpO2）;测空腹血糖,用高度特异的单克隆抗体夹心放大酶联免疫分析法测真胰岛素（TI）,IR的体内稳定状态模式评估方法（HOMA-IR）评估IR;行多导睡眠图（PSG）监测,计算呼吸暂停低通气指数（AHI）。结果同样是肥胖者,肥胖OSAHS组TI、HOMA—IR高于肥胖非OSAHS组,而最低SpO2低于肥胖非OSAHS组;在非OSAHS者中,肥胖非OSAHS组TI、HOMA-IR高于正常体重非OSAHS组,而最低SpO2低于正常体重非OSAHS组。协方差分析校正年龄、BMI、腰臀比的影响后,肥胖OSAHS组的TI、HOMA-IR仍明显高于肥胖非OSAHS组和正常体重非OSAHS组,肥胖非OSAHS组的TI、HOMA—IR明显高于正常体重非OSAHS组。多元线性回归分析显示MTU、HOMA—IR均与年龄和最低SpO2呈负相关,与BMI、腰臀比、AHI呈正相关;当以TU作因变量时,腰臀比是影响肥胖OSAHS组IR的主要因素,AHI与最低SpO2是TI的独立影响因素;当以HOMA—IR作因变量时,腰臀比是其主要影响因素,AHI与最低SpO2是其独立影响因素。结论OSAHS与IR独立相关,OSAHS可能经IR这一中间途径导致心血管疾病。     

采用肥胖参数筛查和诊断老年男性阻塞性睡眠呼吸暂停低通气综合征的研究

目的 应用受试者工作特征曲线(receiver operating characteristic curve,ROC curve)探讨体质指数(BMI)、颈围、腰围及腰臀比等各种肥胖参数筛查、诊断老年男性阻塞性睡眠呼吸暂停低通气综合征(OSAHS)的参考切点并比较其价值. 方法 分析402例老年男性患者的BMI、颈围、腰围及腰臀比与呼吸暂停低通气指数(apnea-hypopnea index,AHI)间的相关性;用ROC曲线确定BMI、颈围、腰围、腰臀比等肥胖参数筛查、诊断OSAHS的参考切点;用ROC曲线下面积(Area under curve,AUC)判断各肥胖参数的整体准确性. 结果 (1)老年男性BMI、颈围、腰围及腰臀比均与AHI呈正相关,其相关系数分别为0.241、0.201、0.210、0.097,P值分别为0.000、0.000、0.000、0.053;BMI、颈围、腰围及腰臀比ROC曲线下面积分别为:0.61、0.58、0.51、0.45,P值分别为0.001、0.060、0.840、0.250;BMI可用于筛查、诊断老年男性OSAHS;颈围、腰围、腰臀比尚不足以用于筛查、诊断老年男性OSAHS;(2)灵敏度达90%,漏诊率10%时,BMI筛查OSAHS的切点为22.0kg/m~2;(3)特异度达90%,误诊率10%时,BMI确诊OSAHS的切点为29.0 kg/m~2. 结论 BMI≥22.0 kg/m~2可作为筛查老年男性OSAHS的参考标准;BMI≥29.0 kg/m~2可作为诊断老年男性OSAHS的参考标准.     

Beta2 adrenoceptor functional gene variants,obesity, and blood pressure level interactions in the general population

We investigated the association of beta2 adrenoceptor functional gene variants (Arg16Gly, Gln27Glu, and Thr164Ile polymorphisms), obesity phenotypes, and blood pressure levels in a large, ethnically mixed urban population. The individuals (n=1576) were randomly selected for a cross-sectional study of cardiovascular risk factors in Vitória, Brazil. Statistically significant associations among systolic blood pressure and the Arg16Gly and Thr164Ile variants were identified in univariate analysis. The Gly16/Gly16 genotype was still associated with systolic blood pressure (SBP) in multivariate analysis adjusting for age, gender, ethnicity, total cholesterol, diabetes, and body mass index (BMI) (P=0.01). The Arg16 allele was the only genotypic variable associated with BMI, and, in a dominant model, it remained associated with an increased BMI even after adjustment for age, gender, ethnicity, triglycerides, HDL cholesterol, LDL cholesterol, diabetes, and hypertension status (P=0.02). Although the different polymorphisms did not interact in the determination of SBP, a significant interaction with BMI (P=0.02), not through linkage disequilibrium, was identified between the Gln27Glu and the Thr164Ile variants. Furthermore, a significant interaction among the Arg16Gly polymorphism and BMI (P=0.036) and waist-hip ratio (P=0.003) in determining SBP was disclosed by ANOVA factorial modeling, with SBP used as the dependent variable. An interaction between the Thr164Ile polymorphism and waist-hip ratio was also identified (P=0.018). Finally, multiple logistic regression models showed a 1.48-fold increase in the risk of hypertension in individuals harboring the Gly16/Gly16 genotype and a 1.31-fold (P=0.01) and a 1.49-fold (P=0.003) increased risk of obesity in individuals harboring the Gln27/Gln27 genotype or the presence of the Arg16 allele, respectively. Taken together, these data provide evidence for a strong but complex relation between beta-adrenoceptor gene variants, hypertension, and obesity.