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1.
目的评价经鼻持续气道正压通气(nCPAP)治疗对阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血清瘦素水平及胰岛素抵抗的影响,探讨OSAHS患者血清瘦素水平和胰岛素抵抗的关系.方法对16例中重度OSAHS患者进行nCPAP治疗,治疗前后进行睡眠监测(PSG),记录睡眠呼吸监测的相关指标,检测空腹血糖(FBG)、空腹血清瘦素及空腹胰岛素水平,采用稳态模型评估法(HOMA)评价并计算胰岛素抵抗指数(HOMA-IR),对比nCPAP治疗前后各指标的差异,并对治疗后空腹血清瘦素水平的变化及胰岛素抵抗的变化与睡眠各参数的变化进行相关分析.结果 nCPAP治疗前后空腹血清瘦素水平有差异(P〈0.01),而HOMA-IR、FBG、胰岛素、BMI差异不明显(P〉0.05),瘦素水平的变化与最低血氧饱和度的变化及AHI的变化呈正相关.结论 nCPAP治疗可降低OSAHS患者的血清瘦素水平,改善睡眠呼吸紊乱,但胰岛素抵抗及空腹血糖无明显变化,治疗后瘦素水平的变化与最低氧饱和度及AHI的改善有关,提示在OSAHS患者中改善睡眠呼吸紊乱的重要性.  相似文献   

2.
目的 研究阻塞性睡眠呼吸暂停低通气综合征(OSAHS)与高血压及瘦素的关系,初步探讨睡眠呼吸紊乱及瘦素在OSAHS并发高血压发病中的作用.方法 测定60例OSAHS及40例年龄、体质指数(BMI)相匹配对照组睡前及醒后血压(BP)、醒后心率(HR),血清瘦素(LEp)水平,同时测定BMI、颈围(NC)、腰臀比(WHR)、血清空腹血糖(FBG)、三酰甘油(TG)、胆固醇(Chol)、空腹真胰岛素(TI)水平.对比两组睡前、醒后BP变化;分析睡眠呼吸紊乱参数及瘦素与高血压的相关关系.结果 OSAHS组与对照组睡前血压差异无显著性(P>0.05),但醒后血压尤其是舒张压(89.75±2.04)mmHg显著高于对照组(81.63±1.91)mmHg并独立于年龄和肥胖(P<0.01);OSAHS组DBP与瘦素、呼吸暂停低通气指数(AHI)呈正相关(r=0.282,P<0.05;r=0.318,P<0.01);BMI(P=0.029)、醒后HR(P=0.030)及瘦素(P=0.049)可能是高血压发生的独立相关因素.结论 睡眠呼吸紊乱可能对醒后血压,尤其是醒后舒张压产生独立的效应;而BMI、醒后HR和瘦素可能是高血压的独立相关因素.  相似文献   

3.
目的 探讨阻塞性睡眠呼吸暂停低通气综合征(obstructive sleep apnea and hypopnea syndrome,OSAHS)患者血清瘦素水平与胰岛素抵抗的关系,以及2者与睡眠呼吸监测各指标的相关性.方法 选择未接受任何治疗的OSAHS患者69例,健康体检者20例为对照组,记录睡眠呼吸监测各项指标,计算体块指数(BMI),同步检测空腹血糖(FBG)、空腹血清瘦素及空腹胰岛素水平,以HOMA-IR评价胰岛素抵抗.(1)据AHI分为正常对照组(10例),轻度OSAHS组(19例),中度OSAHS组(26例),重度OSAHS组(24例);(2)据BMI及AHI分为A组(正常对照10例),B组(单纯肥胖10例),C组(非肥胖OSAHS27例),D组(肥胖OSAHS 42例).分别比较各组间空腹血清瘦素水平、空腹血糖、空腹胰岛素、HOMA-IR的差异; (3)分析OSAHS患者血清瘦素水平与HOMA-IR的相关性,以及2者与空腹血糖、空腹胰岛素、睡眠呼吸监测各项指标的相关性.结果 (1)空腹血清瘦素水平、空腹胰岛素水平、HOMA-IR:重度OSAHS组高于轻中度OSAHS组及正常对照组(P<0.01),B、C、D3组高于A组(P<0.05),D组高于B、C组(P<0.05); (2)空腹血糖:重度OSAHS组高于轻度OSAHS组及正常对照组(P<0.05),B、C、D3组高于A组(P<0.05),D组高于B、C组(P<0.05); (3)轻中度OSAHS组间及B、C组间以上指标差异不明显(P>0.05); (4) OSAHS患者血清瘦素水平与HOMA-IR呈正相关;血清瘦素水平、HOMA-IR与空腹血糖水平、空腹胰岛素、AHI、BMI、ESS呈正相关,与平均血氧饱和度及最低血氧饱和度呈负相关.结论 OSAHS患者血清瘦素及胰岛素抵抗增高,与睡眠呼吸紊乱及低氧存在相关性,胰岛素抵抗与血清瘦素水平的增高有关,OSAHS病情严重度可影响瘦素分泌及胰岛素抵抗.  相似文献   

4.
目的 探讨测定阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血清瘦素水平的临床意义.方法 选择年龄、性别差异无统计学意义的肥胖OSAHS患者65例(肥胖OSAHS组)、非肥胖OSAHS患者39例(非肥胖OSAHS组)、单纯肥胖患者13例(肥胖对照组)和健康人22名(正常对照组)进行多导睡眠图(PSG)监测,用放射免疫法测定所有对象的血清瘦素水平.结果 肥胖OSAHS组血清瘦素水平(17.85±7.86)ng/L较非肥胖OSAHS组(13.42±6.11)ng/L增高(P<0.01);肥胖OSAHS及非肥胖OSAHS组血清瘦素较肥胖对照组(12.25±4.72)ng/L、正常对照组(7.86±2.02)ng/L增高(P<0.05或0.01).OSAHS患者血清瘦素水平较对照组升高(F=7.01,P<0.01),肥胖患者血清瘦素水平较非肥胖者升高(F=17.38,P<0.01),肥胖与OSAHS无交互作用(F=1.44,P>0.05).血清瘦素水平与体重指数(BMI)、微觉醒指数(MAI)、呼吸暂停低通气指数(AHI)、氧减指数(ODI4)呈正相关(r=0.39、0.17、0.24、0.24,P<0.01或0.05). 结论 OSAHS患者、肥胖患者血清瘦素水平增高,除肥胖因素外,OSAHS本身也是引起瘦素水平升高的原因.  相似文献   

5.
目的探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血清瘦素水平及与胰岛素抵抗的相关性.方法选择OSAHS患者和健康者(对照组)各50例,分别行多导睡眠图检查,并测定空腹血糖、瘦素和胰岛素水平.结果 (1)OSAHS患者组的血清瘦素、空腹胰岛素水平及胰岛素抵抗指数(HOMA-IR)与对照组间差别均有显著性意义(P<0.01).(2)OSAHS患者组血清瘦素水平、空腹胰岛素水平、HOMA-IR均与呼吸暂停低通气指数(AHI)、呼吸障碍事件最长时间、微觉醒指数呈正相关,与最低血氧饱和度呈负相关.(3)OSAHS患者血清瘦素水平与空腹胰岛素水平、HOMA-IR呈正相关.结论 (1)OSAHS患者的空腹血清瘦素水平升高,且与OSAHS病情严重程度有关.(2)OSAHS独立于肥胖等混淆因素与胰岛素抵抗存在相关性.(3)OSAHS患者血清瘦素水平与胰岛素抵抗存在相关性.  相似文献   

6.
目的研究血清瘦素在不同糖代谢人群中的水平,并探讨其与胰岛素抵抗(IR)之间的关系。方法纳入糖耐量正常(NGT)者40名(NGT组),糖调节受损(IGR)40例(IGR组)及2型糖尿病(DM)患者40例(2型DM组)。采用放射免疫法检测血清瘦素水平,分析其与各项临床检验指标间关系。结果与NGT组比较,IGR与2型DM组血清瘦素水平均升高[(7.34±1.69)μg/L vs.(9.63±0.61)μg/L、(10.24±0.91)μg/L,P均<0.01],血清瘦素水平与空腹血糖(FPG)、餐后2小时血糖(2 hPG)、收缩压(SBP)、三酰甘油(TG)、空腹胰岛素(FIns)、C反应蛋白(CRP)、体质量指数(BMI)、HOMA-IR水平呈正相关(r=0.068、0.058、0.599、0.578、0.394、0.640、0.340、0.859,P均<0.05),HOAM-IR和FIns是瘦素水平的独立相关因素(t=3.876、4.124,P<0.01)。结论瘦素水平升高与IR密切相关,瘦素可能是2型DM和IGR发生发展的一个促进因素。  相似文献   

7.
目的 探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血浆内脂素水平的变化及其影响因素.方法 选取经多导睡眠监测仪(PSG)整夜监测诊断为中度、重度及极重度OSAHS(AHI>20次/h)的男性患者50例,对照组20例(AHI<5次/h),两组年龄、性别及体质量指数(BMI)相匹配.入选者均检测空腹血糖(FPG)、总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、空腹胰岛素(FINS)和内脂素,测量身高、体重、腰围及臀围,计算BMI、腰臀比和胰岛素抵抗指数(HOMA-IR).结果 OSAHS组血浆内脂素水平明显高于对照组[(45.06±9.17)μg/L vs(36.07±6.53)μg/L,P<0.001];中、重及极重度OSAHS组间血浆脂联素水平差异有显著性(P<0.001);内脂素与腰围、BMI、腰臀比、AHI、血氧饱和度(SaO2)<90%时间百分数、空腹血糖、胰岛素、HOMA-IR、TG及LDL-C均正相关,与平均Sao2、最低Sao2负相关.控制腰围、BMI、腰臀比、空腹血糖、胰岛素、HOMA-IR、TG及LDL-C后,血浆内脂素水平仍与AHI正相关(R'=0.331,P<0.05),与最低SaO2负相关(R'=0.301,P<0.05).多元逐步回归分析表明,AHI是除了腰围以外血浆内脂素的独立影响因素.结论 OSAHS及其严重程度独立影响血浆内脂素水平.  相似文献   

8.
目的研究阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者的睡眠呼吸紊乱指标与其血清瘦素水平和胰岛素抵抗程度的关系。方法选择未接受任何治疗、经多导睡眠监测仪8 h睡眠监测确诊为OSAHS的男性患者54例,参照OSAHS诊治指南按睡眠暂停低通气指数(AHI)进行病情分度,其中轻-中度组(轻度9例,中度18例)和重度OSAHS组各27例,次日监测结束后空腹外周血瘦素、空腹胰岛素和血糖水平,计算体重指数(BMI)(体重/身高2)和HOMA-IR指数[(空腹血糖×空腹胰岛素)/22.5]。结果重度OSAHS组的平均和最低SpO2皆显著低于轻-中度组,BMI、血清瘦素水平和HOMA指数则明显高于轻-中度组,上述指标在两组间比较皆有显著统计学差异(均P<0.01)。其中瘦素与BMI和AHI成正相关,与平均及最低脉氧饱和度均存在负相关。HOMA-IR指数则和BMI、AHI成正相关,和最低SpO2存在负相关。结论在OSAHS患者中,睡眠呼吸功能紊乱和肥胖、瘦素和胰岛素抵抗有关。  相似文献   

9.
目的 探讨阻塞性睡眠呼吸暂停 /低通气综合征 (OSAHS)患者血清瘦素水平的变化及其临床意义。 方法  35例OSAHS患者和 30例健康人 (对照组 ) ,用多导睡眠呼吸监测仪进行夜间 7h睡眠监测 ,睡前及清晨测量血压 ,抽取静脉血放射免疫法测定血清瘦素水平。 结果  (1)OSAHS组空腹血清瘦素水平显著高于对照组[(6 2 4± 1 5 1)ng/mL ,(4 4 1± 1 72 )ng/mL ,P <0 0 1]。平衡体质量指数 (BMI)后 ,差别仍有显著意义 [(6 0 3±1 6 2 )ng/mL ,(4 6 5± 1 34)ng/mL ,P <0 0 5 ]。 (2 )OSAHS组清晨舒张压显著高于睡前 [(89± 12 )mmHg ,(74±14 )mmHg ,P <0 0 1]。 (3)相关分析 ,血清瘦水平与睡眠呼吸暂停 /低通气指数 (AHI) (r =0 4 16 ,P <0 0 1)、体质量指数 (BMI) (r=0 2 93,P <0 0 5 )、SpO2 <90 %的时间 (r =0 385 ,P <0 0 1)呈正相关。对瘦素水平与其相关变量进行多因素逐步回归分析 ,入选变量依次为BMI、AHI、SpO2 <90 %的时间和DBP。 结论 OSAHS患者血清瘦素水平升高 ,且独立于肥胖因素 ,OSAHS本身是引起瘦素水平升高的原因。  相似文献   

10.
目的 观察格列美脲对2型糖尿病(T2DM)患者血清胰岛素样生长因子-1(IGF-1)的影响.方法 采用病例对照及治疗前后自身对照研究,检测T2DM患者治疗前空腹血清IGF-1的水平及格列美脲治疗6个月后的改变情况.其中T2DM组54例,正常对照组90例.结果 与正常对照组相比,T2DM组治疗前血清IGF-1水平明显下降[(42.5±9.2)μg/L vs (74.2±10.6)μg/L,P<0.01];经格列美脲治疗后T2DM组血清IGF-1水平较治疗前明显升高[(62.5 ±8.4)μg/L vs (42.5±9.2)μg/L,P<0.05].结论 格列美脲治疗可改善T2DM所导致的IGF-1水平改变.  相似文献   

11.
目的探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)及其合并代谢综合征(MS)患者血清瘦素(Lep)的变化及意义。方法OSAHS男性患者70例,分为单纯OSAHS组40例及OSAHS合并MS组30例,40例年龄、体质量指数(BMI)与OSAHS患者相匹配者为对照组,测量身高、体质量、颈围(NC)、腰围、臀围等,检测各组血清空腹血糖(FBG)、血清瘦素(Lep)、空腹真胰岛素(TI)水平、三酰甘油(TG)、胆固醇(Ch01),采用稳态模型评估法(nOMA)评价并计算胰岛素抵抗指数(HOMA—IR)。结果①OSAHS组与OSAHS组合并MS组患者血清Lep水平高于对照组(P〈0.05,P〈0.01),且OSAHS合并Ms纽血清Lep高于OSAttS组(P〈0.01),OSAHS纽亚组间,中、重度组高于轻度组(P〈0.05,P〈0.01)。②血清Lep水平与其他指标的Spearman’s相关分析:OSAHS组血清Lep水平与AHI、HOMA—IR、BMI呈正相关(P〈0.01),与最低氧饱和度(LSpO2)呈负相关(P〈0.01)。OS—AHS合并MS组血清Lep水平与呼吸暂停低通气指数(AHI)、HOMA—IR、BMI、NC、腰臀比(WHR)、收缩压(SBP)、舒张压(DBP)、FBG、TG等呈显著正相关(P〈0.001),与最低氧饱和度(LSpO2)呈负相关(P〈0.001),多元线性逐步回归分析显示:BMI(P=0.003)、HOMA—IR(P=0.024)、AHI(P=0.036)是OSAHS组血清瘦素水平的独立相关因素。③OSAHS组与BMI、年龄相匹配的对照组相比醒后血压,尤其是舒张压要高于对照组(P〈0.01);各组血压与各指标进行Spearman’s相关分析示:与BMI、AHI、Lep正相关;多元Logistic回归分析表明:BMI(P=0.031)及Lep水平(P=0.064)是高血压的独立相关因素。结论OSAHS较单纯肥胖者有更高的瘦素水平,与OSAHS进展有关,高瘦素血症并存胰岛素抵抗可能参与了OSAHS合并MS的病理生理过程。  相似文献   

12.
目的探讨胰岛素抵抗(IR)、瘦素和阻塞性睡眠呼吸暂停低通气综合征(OSAHS)的关系。方法检测并分析对照组、肥胖的轻度OSAHS组、肥胖的中重度OSAHS组、非肥胖的轻度OSAHS组和非肥胖的中重度OSAHS组的体重指数、颈围、腰围、HOMA2-IR、血清瘦素水平和血脂系列。结果(1)肥胖的轻度、中重度OSAHS组和非肥胖的中重度OSAHS组的HOMA2-IR、瘦素高于对照组(P〈0.01)。肥胖和非肥胖的中重度OSAHS组的HOMA2-IR、瘦素均高于相应的轻度OSAHS组(P〈0.01)。(2)瘦素与HOMA2-IR、AHI、BMI、颈围、腰围、TG呈正相关(P〈0.05—0.001),与HDL—C呈负相关(P〈0.05)。HOMA2-IR与瘦素、BMI、颈围、腰围、AHI呈正相关(P〈0.001),与HDL—C呈负相关(P〈0.05)。(3)多元逐步回归分析,得出影响瘦素的因素依次是AHI、BMI、CH;影响HOMA2-IR的因素依次是瘦素、BMI和AHI。结论OSAHS是影响IR、血清瘦素水平的独立危险因素,高瘦素水平是影响IR的重要危险因素。  相似文献   

13.
Ye CX  Gao XL  Ou Q  Li DF  Cen RJ  Zhou MH 《中华医学杂志》2007,87(31):2181-2184
目的:探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血管内皮细胞的损伤机制。方法:按多导睡眠监测仪检查结果将研究对象分为正常对照组(n=20)、轻度OSAHS组(n=21)、中度OSAHS组(n=24)和重度OSAHS组(n=20)。所有研究对象睡醒后(约6点30分左右)采外周静脉血,分离单个核细胞(MNC)。分离的MNC与人脐静脉内皮细胞ECV304共同培养48h,培养后收集上清液及内皮细胞,ELISA检测上清液中的TNF-α、IL-6,流式细胞仪检测内皮细胞的凋亡率、Fas蛋白表达。结果:正常对照组、轻、中及重度OSAHS患者MNC细胞产生肿瘤坏死因子α(TNF-α)分别为(0.80±0.10)μg/L、(1.20±0.30)μg/L、(1.40±0.50)μg/L及(2.10±0.60)μg/L,多组比较(F=69.65,P〈0.01);产生白细胞介素6(IL-6)分别为(23.50±6.50)μg/L、(49.60±2.80)μg/L、(46.90±10.80)μg/L及(64.80±9.90)μg/L,多组比较(F=182.83,P〈0.01)。MNC细胞产生TNF-α及IL-6均高于正常对照组(均P〈0.01);而重度OSAHS患者MNC产生TNF-α及IL-6均高于轻度及中度(均P〈0.01),轻度与中度OSAHS患者之间差异无统计学意义。内皮细胞的凋亡率:正常对照组、轻、中及重度OSAHS患者分别为8.3%±3.2%、9.2%±3.0%、19.3%±6,3%及19.6%±3.8%,多组比较(F=39.36,P〈0.01);中、重度OSAHS患者较正常对照组升高(P〈0.01);而轻度OSAHS患者与正常对照组比较,中度与重度OSAHS患者组比较,差异均无统计学意义。内皮细胞表达Fas蛋白各组问差异无统计学意义。内皮细胞凋亡率与OSAHS患者AHI呈正相关(r=0.58913,P=0.0106)、与夜间最低血氧饱和度呈负相关(r=-0.50737,P〈0.01)。结论:OSAHS患者血管内皮细胞损伤过程中,单个核细胞可能起重要作用,且这种作用同病情严重程度、夜间缺氧密切相关。  相似文献   

14.
Adipocytokines and breast cancer risk   总被引:6,自引:0,他引:6  
Hou WK  Xu YX  Yu T  Zhang L  Zhang WW  Fu CL  Sun Y  Wu Q  Chen L 《中华医学杂志(英文版)》2007,120(18):1592-1596
Background Many researches suggested that obesity increased the risk of breast cancer, but the mechanism was currently unknown. Adipocytokines might mediate the relationship. Our study was aimed to investigate the relationship between serum levels of resistin, adiponectin and leptin and the onset, invasion and metastasis of breast cancer. Methods Blood samples were collected from 80 newly diagnosed, histologically confirmed breast cancer patients and 50 age-matched healthy controls. Serum levels of resistin, adiponectin and leptin were determined by enzyme-linked immunosorbent assays (ELISA); fasting blood glucose (FBG), lipids, body mass index (BMI), and waist circumference (WC) were assayed simultaneously.Results Serum levels of adiponectin ((8.60±2.92) mg/L vs (10.37±2.81) mg/L, P=0.001) and HDL-c were significantly decreased in breast cancer patients in comparison to controls. Serum levels of resistin ((26.35±5.36) μg/L vs (23.32±4.75) μg/L, P=0.000), leptin ((1.35±0.42) μg/L vs (1.06±0.39) μg/L, P=0.003), FBG and triglyceride (TG) in breast cancer patients were increased in contrast to controls, respectively. However, we did not find the significant difference of the serum levels of resistin, adiponectin and leptin between premenopausal breast cancer patients and healthy controls (P=0.091, 0.109 and 0.084, respectively). The serum levels of resistin, adiponectin and leptin were significantly different between patients with lymph node metastasis (LNM) and those without LNM (P=0.001, 0.000 and 0.006, respectively). The stepwise regression analysis indicated that the tumor size had the close correlation with leptin (R(2)=0.414, P=0.000) and FBG (R(2)=0.602, P=0.000). Logistic regression analysis showed that reduced serum levels of adiponectin (OR: 0.805; 95%CI: 0.704–0.921; P=0.001), HDL (OR: 0.087; 95%CI: 0.011–0.691, P=0.021), elevated leptin (OR: 2.235; 95%CI:1.898–4.526; P=0.004) and resistin (OR: 1.335; 95%CI: 1.114–2.354; P=0.012) increased the risk for breast cancer; Reduced serum levels of adiponectin (OR: 0.742; 95%CI: 0.504–0.921; P=0.003) and elevated leptin (OR: 2.134; 95%CI:1.725–3.921; P= 0.001) were associated with lymph node metastasis of breast cancer. Conclusions The decreased serum adiponectin levels and increased serum resistin and leptin levels are risk factors of breast cancer. The low serum adiponectin levels and high serum leptin levels are independent risk factors for metastasis of cancer. The association between obesity and breast cancer risk might be explained by adipocytokines.  相似文献   

15.
Background Adiponectin, secreted by adipocytes, has been found to be associated with diabetes, obesity and some cardiovascular diseases. Obstructive sleep apnea hypopnea syndrome (OSAHS) is also closely related to obesity and easily complicated with diabetes and some cardiovascular diseases. This study was carried out to explore the change of serum adiponectin level in patients with OSAHS.Methods Polysomnography was performed in 71 patients with OSAHS (OSAHS group) and 26 simple obese controls (control group). The two groups had no significant difference in age and body mass index (BMI). Radioimmunoassy was used to test serum adiponectin level.Results Serum adiponectin level was significantly lower in OSAHS group [(5.03±1.01) mg/L] than that in the control group [(7.09±1.29) mg/L, P&lt;0.05]. The differences between two groups were independent of gender. In OSAHS groups, serum adiponectin levels were negatively correlated with apnea hypopnea index (AHI) (r=-0.78, P&lt;0.01), BMI (r=-0.13, P&lt;0.05), waist circumsference (r=-0.36, P&lt;0.01), and neck circumference (r=-0.42, P&lt;0.01), but positively correlated with the minimal pulse oxyhemoglobin saturation (r=0.48, P&lt;0.01). Conclusion OSAHS may contribute to the decrease of serum adiponectin level independent of obesity.  相似文献   

16.
Leptin, the adipocyte-specific product of the ob gene, is implicated in body weight regulation and energy balance. We investigated the influence of hormone replacement therapy (HRT) on the body mass index (BMI) and serum leptin levels in 20 postmenopausal, nonobese women treated with transdermal HRT (delivery rate 50 microg 17beta-estradiol/24 h, 1 patch per week) for 6 months. Serum leptin levels were measured by ELISA and results were compared by means of the Student's paired t-test or Pearson's correlation. The mean patient age was 55+/-6.04 years. The mean body weight prior to the start of the study was 69.39+/-9.37 kg, and the BMI before HRT was 26.92+/-4.47 kg/m2. Both parameters remained unchanged under therapy. No significant change in absolute serum leptin values (18.8+/-8.4 ng/ml; 20.47+/-9.7 ng/ml; 17.92+/-8.7 ng/ml at 0, 4 and 6 months respectively) or in adiposity-corrected values (serum leptin/BMI) (0.68+/-0.24; 0.75+/-0.29; 0.67+/-0.26 at 0, 4 and 6 months respectively) were found. Serum leptin levels correlated well with BMI (r = 0.7193, p<0.0001). There was no significant correlation of estradiol with serum leptin levels before or during therapy. In summary, low dose, transdermal HRT exhibited no influence on serum leptin levels or BMI in postmenopausal women. These data suggest that low dose HRT does not influence body weight regulation in postmenopausal women.  相似文献   

17.
血清瘦素水平与原发性高血压的相关性研究   总被引:25,自引:0,他引:25  
Li M  Wu CY  Zhan ZW  Yang J  Zhang K  Li XG  Gan LH  Ji BH 《中华医学杂志》2003,83(12):1058-1061
目的 探讨瘦素、肥胖、胰岛素抵抗与血压的相互关系 ,评价瘦素在高血压发病中的作用。方法  5 6 0名非糖尿病的成年男性 ,测定空腹血脂、瘦素、真胰岛素 (TI)浓度以及空腹和餐后 2h血糖。胰岛素敏感性以稳态模型抵抗指数 (HOMA R)评价。结果 空腹瘦素水平与体重指数 (BMI)、腰臀比 (WHR)、TI和HOMA R、血压以及甘油三酯和胆固醇均显著相关 (均为P <0 0 1)。在调整年龄、BMI、WHR和HOMA R后 ,瘦素仍与收缩压呈正相关 (r=0 11,P <0 0 5 ) ,而且高血压者 (除外服用降压药者 )的瘦素水平也显著高于非高血压者 (几何均值 6 4 μg/L对 4 7μg/L ,P <0 0 0 1)。肥胖、胰岛素抵抗和高瘦素血症均能明显增加高血压的检出率。Logistic回归分析也显示瘦素水平的升高与高血压的发病密切相关。结论 瘦素与肥胖型高血压的发病相关。  相似文献   

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