阻塞性睡眠呼吸暂停综合征老年患者血管内皮功能变化及其与冠心病的关系

目的　探讨老年阻塞性睡眠呼吸暂停综合征 (OSAS)患者血管内皮功能变化与冠心病 (CHD)的内在联系。方法　随机选择 31例无OSAS、无心血管疾病的老年单纯鼾症者为对照组 ,4 5例老年中、重度OSAS患者为OSAS组 ,OSAS组内又分为有CHD(16例 )和无CHD(2 9例 )两个亚组。测定和比较组间的血浆一氧化氮 (NO)、内皮素 (ET)及其比值的动态变化及OSAS组内CHD有无的区别。结果　与对照组相比 ,OSAS组患者的NO水平明显降低〔(2 7.6 9± 9.17)vs(6 1.90± 13.4 7) μmol/L〕 ,ET水平明显增高〔(5 8.0 8± 14 .2 1)vs (34.77± 8.2 3)ng/L〕 ,NO/ET比值明显下降〔(0 .4 7± 0 .18)vs (1.72± 0 .97) ,均P <0 .0 1)〕。CHD的发生率在OSAS组达 35 .6 %。与对照组相比 ,OSAS组中不伴CHD者降低的NO水平 (35 .5 3± 9.39) μmol/L、升高的ET水平 (47.78± 11.13)ng/L和下降的NO/ET比值 (0 .75± 0 .13)已有显著性差异 (P <0 .0 5 ) ;伴有CHD者的NO水平 (2 2 .17± 8.76 )μmol/L、ET水平 (6 9.14± 12 .17)ng/L和NO/ET比值 (0 .32± 0 .14 )较对照组相差更为明显 (P <0 .0 1)。结论　OSAS老年患者存在明显的血管内皮功能障碍 ,尤以CHD者为甚 ,血管内皮功能损伤可能是OSAS患者并发CHD的原因     

阻塞性睡眠呼吸暂停患者血清肿瘤坏死因子水平及与血脂的关系

目的探讨阻塞性睡眠呼吸暂停综合征(OSAS)患者血清肿瘤坏死因子(TNFα)水平及与脂肪代谢的关系。方法选择OSAS患者58例,单纯肥胖患者21例,分别应用酶联免疫法(ELISA)测定血清TNFα,应用生化酶法测定血脂水平,分析OSAS患者TNFα与血脂以及病情的关系。结果OSAS患者血清TNFα水平〔(291.1±146.2)pmol/L〕高于对照组〔(196.0±86.5)pmol/L〕,血清胆固醇、甘油三酯升高,甘油三酯变化与TNFα水平具有相关性(r=0.575,P<0.01)。结论OSAS患者血清TNFα水平明显升高,并与血脂水平相关。     

冠心病与阻塞性睡眠呼吸暂停综合征患者睡眠动脉血氧减饱和度指数分析

目的 :探讨阻塞性睡眠呼吸暂停综合征 (OSAS)与冠心病 (CHD)发生、发展的关系。方法 :通过使用多导睡眠仪对 38例单纯 OSAS患者、2 2例 CHD并发 OSAS患者进行氧减饱和度指数 (ODI)监测分析。结果 :CHD并发 OSAS组的 ODI最高为 50 .55± 1 8.2 5,较 OSAS组 (38.65±1 4.2 8)明显增高 (P <0 .0 5) ,且与呼吸紊乱指数呈明显的正相关 (P <0 .0 1 )。结论 :OSAS并发CHD组夜间缺氧程度最重、最频繁 ,OSAS患者 CHD的发生可能与长期低氧有关     

阻塞型睡眠呼吸暂停综合征与胰岛素抵抗的关系

目的　探讨阻塞型睡眠呼吸暂停综合征 (OSAS)低氧与胰岛素抵抗之间的关系及持续正压通气 (CPAP)治疗OSAS对胰岛素抵抗的影响。方法　分析 6 1例OSAS患者CPAP治疗前后及 16例未治疗OSAS患者多导睡眠监测各项指标与空腹血糖、胰岛素和餐后 2h血糖、胰岛素的关系 ,另选择 5 6例不符合SAS诊断者为对照组。结果　OSAS组治疗前呼吸紊乱指数 ( 36 .4±18.2 )次 /h ,最低氧饱和度 ( 74.5± 6 .2 ) % ,餐后血糖 ( 10 .6± 2 .4)mmol/L ,餐后胰岛素 ( 6 9.7±2 7.7)uIU/ml,胰岛素敏感性 ( 0 .8± 0 .2 )。CPAP治疗第 10天复查上述各项指标结果分别为 ( 3.3± 3.4)次 /h、( 86 .5± 1.3) %、( 7.2± 0 .6 )mmol/L、( 39.7± 10 .2 ) μIU/ml、1.2± 0 .2。P值分别 <0 .0 1、<0 .0 1、<0 .0 5、<0 .0 1、<0 .0 1。结论　OSAS组治疗前血浆胰岛素和血糖比对照组高 ,治疗后OSAS组比未治疗组低。表明OSAS低氧可产生胰岛素抵抗。     

老年人阻塞性睡眠呼吸暂停综合征与心脑血管病关系的探讨

目的　分析老年人阻塞性睡眠呼吸暂停综合征 (OSAS)相关事件与心、脑血管疾病发病的关系 ,并探讨其发病机制。　方法　采用多导睡眠图 (PSG)监测 ,筛查出OSAS患者 180例 ,分为老年组 97例和非老年组 83例 ,并设老年对照组 82例。观察血压、血糖、血脂、血浆降钙素基因相关肽(CGRP)、内皮素 (ET)等指标 ,并对心、脑血管疾病患病情况进行随访观察 3年。　结果　 (1)老年人反应性差 ,OSAS常见症状与老年人衰老症状相混淆 ,且与多种疾病并存 ,诊断、治疗具有特殊性。 (2 )老年OSAS组PSG监测 ,呼吸紊乱次数 (34 4± 38)、呼吸紊乱指数 (5 9± 10 )、平均呼吸暂停时间 (35± 13)s、最长呼吸暂停时间 (87± 2 6 )s及平均动脉压 (145± 14)mmHg明显高于对照组 (P <0 0 1) ;最低动脉血氧饱和度 (5 5± 13) %明显低于对照组 (P <0 0 1) ,但老年人重症患者少。 (3)OSAS组血糖、血脂、纤维蛋白原、血浆ET均高于对照组 (P <0 0 1) ;血浆CGRP明显低于对照组 (P <0 0 1)。 (4 ) 3年随访中 ,老年OSAS组心血管疾病 78例 ,患病率 80 4 1%;脑血管疾病 6 5例 ,患病率 6 7 0 1%,明显高于非老年组及老年对照组 ,差异有显著性 (P <0 0 1)。　结论　OSAS与心、脑血管病的发病有密切关系 ,是引起OSAS的危险因素之一 ,进一步     

阻塞性睡眠呼吸暂停低通气综合征患者血浆食欲素A水平的变化及意义

目的探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血浆食欲素A的变化及意义。方法选择OSAHS并肥胖患者30例(OSAHS组)、单纯肥胖者30例(单纯肥胖组)和健康成人20名(正常对照组)。其中OSAHS组和单纯肥胖组的体重指数(BMI)均≥25kg/m2且差异无统计学意义。所有受试者均接受多导睡眠仪监测,采用层析及放射免疫法测定血浆食欲素A的水平。结果OSAHS组血浆食欲素A水平[(9.0±1.8)ng/L]显著高于单纯肥胖组[(7.2±1.4)ng/L,P<0.01]及正常对照组[(6.7±1.6)ng/L,P<0.01]。OSAHS组血浆食欲素A水平与呼吸暂停低通气指数(AHI)、微觉醒指数(arousalindex)呈正相关(r=0.639、0.435,P均<0.05),与最低血氧饱和度(LSaO2)、平均血氧饱和度(MSaO2)呈负相关(r=-0.521、-0.589,P均<0.01)。OSAHS组及单纯肥胖组血浆食欲素A水平与BMI无相关性(r=0.132,P>0.05)。结论OSAHS患者血浆食欲素A水平升高,其原因可能与患者夜间反复发作性低氧有关,且食欲素A在调节睡眠觉醒的过程中可能发挥了重要的作用。     

阻塞性睡眠呼吸暂停低通气综合征患者血清铁蛋白、铁调素的变化及其临床意义

目的 探讨阻塞性睡眠呼吸暂停低通气综合征(OSAS)患者血清铁蛋白(SF)、铁调素的变化及其临床意义.方法 选取经多导睡眠监测确诊为OSAS的男性患者51例,其中单纯OSAS组36例(轻度OSAS组13例,中重度OSAS组23例),OSAS合并糖尿病组15例；另选取单纯2型糖尿病(T2DM)患者14例作为T2DM组；设立单纯肥胖男性18例为对照组.分别检测各组受试者空腹血糖、HbA1c及空腹胰岛素水平,并用ELISA法检测SF、铁调素水平,观察OSAS患者SF、铁调素对糖代谢的影响.结果 (1)轻度OSAS组、中重度OSAS组、OSAS合并糖尿病组和T2DM组的SF水平升高,分别为(268.24±47.94),(316.45 ±49.36),(377.66±49.95),(286.01 ±45.53) μg/L,均高于对照组(203.28±32.83) μg/L,差异有统计学意义(F =39.38,P ＜0.01)；铁调素水平下降,分别为(66.41 ±12.00),(47.34 ±13.35),(34.52±8.49),(54.45±8.25) μg/L,均低于对照组(88.26±12.34)μg/L,差异有统计学意义(F=67.80,P＜0.01).(2)SF、铁调素与睡眠呼吸紊乱指数、最长呼吸暂停时间、夜间血氧饱和度低于90％的时间占总睡眠时间的百分比、最低血氧饱和度存在相关性(r=-0.65 ～0.34,P均＜0.01),且SF与铁调素之间存在线性相关(F=22.40,P＜0.01).结论 OSAS患者存在SF及铁调素水平的异常,可能在T2DM的发生中发挥一定的作用.     

慢性阻塞性肺疾病患者血清抵抗素和瘦素水平及其与营养状况的关系

目的探讨慢性阻塞性肺疾病(COPD)患者血清抵抗素、瘦素水平及其与营养状况的关系。方法用酶联免疫吸附测定(ELISA)和放射免疫法检测57例稳定期COPD患者和31名健康对照者血清抵抗素、瘦素水平,分析相关因素。结果COPD患者血清抵抗素、瘦素水平[(2·1±1·2)、(0·65±0·41)μg/L]与对照组[(3·6±2·3)、(1·03±0·71)μg/L]比较差异均有统计学意义(P均<0·01)。COPD营养不良患者抵抗素、瘦素水平[(1·7±0·7)、(0·43±0·16)μg/L]显著低于非营养不良患者[(2·2±1·2)、(0·73±0·48)μg/L,P均<0·05]。COPD患者抵抗素与瘦素、第一秒用力呼气容积(FEV1)及FEV1/用力肺活量(FVC)显著正相关(r=0.426~0.531,P均<0·01),瘦素与体重指数(BMI)、胸围、腹围、抵抗素及FEV1/FVC显著正相关(r=0.371~0.580,P均<0·01)。结论COPD稳定期患者血清抵抗素、瘦素水平下降,合并营养不良时下降更显著。     

肥胖青少年血清瘦素、胰岛素和胰岛素原水平的变化

目的　检测肥胖青少年血清瘦素、胰岛素、胰岛素原水平的变化 ,探讨青少年肥胖与代谢综合征的关系。方法　从年龄 14～ 16岁的 2 2 17例学生中筛选出体重指数 (BMI)≥ 2 5kg/m2 的肥胖学生 (肥胖组 ) 198例 ,BMI在 18 5～ 2 3 0kg/m2 之间的体重正常学生 (正常组 ) 78例 ,用放射免疫方法测定血清瘦素、胰岛素和胰岛素原水平 ,同时测定血糖及血脂水平 ,比较两组间差异。结果　血清瘦素水平女生明显高于同龄男生 [(18 5 3± 1 4 1) μg/L比 (6 33± 1 79) μg/L]。肥胖组血清瘦素、胰岛素和胰岛素原水平均高于同龄体重正常者 [分别为 (19 94± 1 91) μg/L比 (11 2 7± 2 0 4 ) μg/L ,(15 34± 1 6 6 ) μIU/L比 (13 17± 1 4 3) μIU/L ,(16 19± 1 6 4 )pmol/L比 (11 79± 1 70 )pmol/L ],血糖、甘油三酯 (TG)和高密度脂蛋白胆固醇 (HDL C)水平虽然在正常范围内 ,但肥胖者血糖和TG水平高于同龄体重正常者 [分别为 (4 6 3± 0 5 0 )mmol/L比 (4 13± 0 33)mmol/L ,(1 2 0± 0 5 6 )mmol/L比 (0 90±0 32 )mmol/L],HDL C水平低于同龄体重正常者 [(1 14± 0 2 4 )mmol/L比 (1 38± 0 2 6 )mmol/L]。结论　肥胖青少年可能存在瘦素抵抗、胰岛素抵抗及潜在的糖代谢和脂代谢异常等代谢综合征改变 ,     

持续气道正压通气治疗对OSAHS患者呼出气冷凝液和血清中瘦素水平的影响

目的 探讨自动调节持续气道正压通气(auto-CPAP)治疗对阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者呼出气冷凝液(EBC)和血清中瘦素水平的影响.方法 根据多导睡眠监测确诊的42例中重度OSAHS患者,随机分为治疗组22例和对照组20例,对治疗组进行三个月auto-CPAP治疗,对治疗组和对照组患者均采取常规治疗,分别测定治疗组及对照组三个月前后EBC和血清中的瘦素.结果 ①治疗组患者EBC和血清中瘦素治疗前[(5.67±1.07) μg/L、(40.20±5.40)μg/L]高于治疗后[(3.75±1.09)μg/L、(30.46±5.82)μg/L](P＜0.01);②对照组患者EBC和血清中Lep治疗前为[(5.52±1.14) μg/L、(42.19±4.96) μg/L],治疗后为[(5.95±1.26) μg/L、(42.69±4.33)μg/L],治疗前后差异无统计学意义(P＞0.05);③OSAHS患者EBC和血清中瘦素水平与呼吸暂停低通气指数呈正相关(r=0.787,P＜0.01; r=0.775,P＜0.01),与最低血氧饱和度、平均血氧饱和度呈负相关(r=-0.829,P＜0.01;r=0.794,P＜0.01)、(r=-0.890,P＜0.01;r=-0.830,P＜0.01).结论 OSAHS患者存在高瘦素血症,auto-CPAP治疗可以改善OSAHS患者的高瘦素血症.     

Leptin and ghrelin levels in patients with obstructive sleep apnea syndrome

BACKGROUND: Leptin is a hormone with well-investigated functions concerning body composition, energy homeostasis and feeding behavior in humans. The obstructive sleep apnea syndrome (OSAS) is strongly associated with obesity, which is known to be closely associated with hyperleptinemia. More recently, ghrelin, a hormone that also influences appetite and energy homeostasis, has been discovered. OBJECTIVES: The aim of this study was to investigate serum leptin and ghrelin levels in obese patients with OSAS in comparison with equally obese controls without OSAS. METHODS: Thirty untreated obese patients with moderate-severe OSAS (apnea-hypopnea index: AHI > or =15) and 22 obese controls (AHI <5) were studied. To confirm the diagnosis, all patients underwent standard polysomnography in our sleep disorders center. Serum samples were taken at 08:00 h in the morning after overnight fasting. RESULTS: Significantly higher serum leptin levels were found in OSAS patients compared to controls (p = 0.012), but there was no significant difference in serum ghrelin levels between OSAS patients and controls. Serum leptin levels were significantly correlated with body mass index in both OSAS patients (r = 0.55, p = 0.002) and controls (r = 0.46, p = 0.028), but only in OSAS patients was the leptin level significantly correlated with AHI (r = 0.38, p = 0.036). CONCLUSION: These data support findings suggesting that leptin is a hormonal factor affected by OSAS and not determined by obesity alone. Further studies are needed to investigate the relationship between serum ghrelin and OSAS.     

阻塞性睡眠呼吸暂停低通气综合征患者血清脂联素水平的研究

目的 探讨血清脂联素在阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者体内的变化。方法 选择伴有肥胖的OSAHS患者71例(肥胖OSAHS组)、不伴肥胖的OSAHS患者21例(非肥胖OSAHS组)、单纯性肥胖者26例(单纯性肥胖组)和健康成人22例(正常对照组)。其中肥胖OSAHS组和单纯性肥胖组的体重指数(BMI)均大于25,两组间BMI差异无显著性。肥胖OSAHS组又进一步分为轻度(26例)、中度(22例)和重度(23例)。均接受多导睡眠仪监测和放射免疫法测定血清脂联素水平。结果 正常对照组血清脂联素水平[(8.9±0.6)mg/L]显著高于单纯性肥胖组[(7.1±1.3)mg/L](P<0.05)、非肥胖OSAHS组[(5.4±0.6)mg/L,P<0.01]和肥胖OSAHS组[(5.0±1.0)mg/L,P<01]。与单纯性肥胖组的血清脂联素水平相比,无论肥胖OSAHS组或非肥胖OSAHS组均显著降低,差异有显著性(P<0.05)。肥胖OSAHS组与非肥胖OSAHS组的血清脂联素水平相比,差异无显著性(P>0.05)。肥胖OSAHS组与单纯性肥胖组的分析显示:血清脂联素水平与呼吸暂停低通气指数(AHI)(r=-0.78,P<0.01)、BMI(r=-0.21,P<0.05)、腰围(r=-O.36,P<0.01)和颈围呈负相关(r=-0.42,P<0.01),与最低脉搏血氧饱和度呈正相关(r=0.48,P<0.01)。结论 OSAHS患者中血清脂联素水平较正常对照和单纯肥胖者更低,除了腰围和颈围的因素     

血清瘦素对慢性阻塞性肺疾病患者营养状态影响的初步研究

目的 探讨血清瘦素及肿瘤坏死因子α（ＴＮＦ－α）的慢性阻塞性肺疾病（ＣＯＰＤ）患者营养不良发生中的意义。方法 测定３１例ＣＯＰＤ患者（分为营养不良组１２例,非营养不良组１９例）及１１名正常人的血清瘦素、ＴＮＦ－α浓度、体重指数（ＢＭＩ）、理想体重百分比（ＮＷ％）、三头肌皮皱厚度（ＴＳＦ）、肩胛下皮皱厚度（ＳＳＦ）、上臂中部臂围（ＭＡＣ）,血清白蛋白（ＡＬＢ）、总淋巴细胞计数（ＬＹＭ）等指标。瘦素与     

老年男性阻塞性睡眠呼吸暂停综合征患者血清脂联素水平的变化

目的探讨老年男性阻塞性睡眠呼吸暂停综合征(OSAS)血清脂联素水平的变化。方法选择62例习惯性打鼾老年人行多导睡眠仪监测,根据呼吸暂停低通气指数(AHI)分为单纯打鼾组(对照组),OSAS组,以放射免疫法测定血清中脂联素水平。结果OSAS组的血清脂联素水平显著低于对照组(P<0.01)。而血清脂联素水平在轻度OSAS患者中即有显著降低(P<0.05),在中度和重度OSAS患者中进一步降低(P<0.01)。OSAS各亚组间的比较发现:中、重度组的血清脂联素水平均明显低于轻度OSAS组(P<0.05)。Pearson相关分析提示OSAS患者血清脂联素水平与AHI、体重指数(BMI)、腰围(WC)、颈围(NC)、反应性胰岛素抵抗的体内稳态模式(HOMA)指数呈负相关,与最低血氧饱和度(mini SpO2)呈正相关。偏相关分析提示血清脂联素水平与AHI呈负相关(r=-0.26,P<0.05),与SpO2呈正相关(r=0.24,P<0.05)。多元逻辑回归分析提示血清脂联素水平与OSAS独立相关。结论老年男性OSAS患者血清中脂联素水平较单纯打鼾者为低。     

Leptin levels in relation to body composition and insulin concentration in patients with endogenous Cushing's syndrome compared to controls matched for body mass index

Cushing's syndrome (CS) is associated with weight gain and visceral obesity. We examined the relationship between regional fat distribution and serum levels of leptin, cortisol and insulin. Twenty-three consecutive patients with recently diagnosed CS (18 with pituitary adenoma, 5 with adrenal tumor), where compared to obese controls, matched for age, sex and Body Mass Index (BMI). Serum insulin, leptin, cortisol, C-peptide and body composition determined by DEXA were measured. Serum leptin levels were significantly increased in patients with CS (36.9+/-3.8 vs 18.9+/-2.4 ng/ml, p<0.001; women: 40.1+/-4.6 vs 21.7+/-2.9 ng/ml, p<0.01; men: 27.9+/-5.7 vs 10.9+/-2.3 ng/ml; p<0.05), the same were fasting insulin levels (178+/-30 vs 81+/-10 pmol/l; p<0.01) and C-peptide (1.51+/-0.12 vs 0.77+/-0.07 nmol/l; p<0.001). In a subgroup of 12 patients, truncal fat mass was significantly elevated when compared to obese controls (19.2 kg vs 14.7 kg, p<0.01, and 42% vs 36% in percentage of truncal body tissue, p<0.05), whereas total fat mass was insignificantly increased. Serum leptin correlated positively to total body fat (%) as in patients with CS (r=0.94, p<0.001) as in controls (r=0.68, p<0.01). The correlation to truncal body fat (%) was also significant in both groups (CS: r=0.84, p<0.001; controls: r=0.63, p<0.01). Multiple regression showed that percent total body fat was the predictor of leptin concentrations among patients with CS (r2=0.88, p<0.001) whereas insulin did not contribute significantly to the variance in leptin concentrations. In controls, both leptin and insulin (r2=0.65, p<0.001) contributed significantly to the variations in leptin levels. Controlled for the differences in total body fat, patients with endogenous CS have significantly increased serum leptin levels, compared to BMI-matched obese controls. This suggests that hyperleptinemia in CS not primarily reflects changes in body composition, but is the result of different hormonal influences on adipose tissue.     

Effect of weight loss and regional fat distribution on plasma leptin concentration in obese women.

OBJECTIVES: To investigate how circulating leptin concentrations are related to regional fat distribution and whether moderate weight loss alters these relationships. DESIGN: A 6 month, clinical weight reduction trial with measurements before and after weight loss. SUBJECTS: 38 healthy, obese women (age: 44.3+/-9.9 y, BMI: 34.0+/-4.0 kg/m2). MEASUREMENTS: The following measurements were made. 1. indices of obesity and fat distribution: weight, body mass index (BMI), hip circumference (peripheral fat), waist circumference, total body fat (bioelectrical impedance), abdominal fat distribution: visceral fat and abdominal subcutaneous fat (ultrasonography); and 2. Biochemical measurements: plasma leptin and serum insulin. RESULTS: Baseline plasma leptin concentrations were three-fold higher in obese women than in normal weight controls. After weight loss averaging 8.4 kg (9.0%), plasma leptin decreased by a mean of 22.3% (P < 0.001), corresponding to body fat decrease of 16.6% (P < 0.001), abdominal subcutaneous fat decrease of 17.4% (P < 0.001) and visceral fat decrease of 18.7% (P < 0.001). The total amount of body fat correlated with plasma (serum) leptin before (r = 0.64, P < 0.001) and after (r = 0.75, P < 0.001) weight loss. Plasma leptin concentrations expressed per kg of body fat did not change significantly during weight loss. After controlling for body fat, baseline leptin concentrations were significantly associated with hip circumference (r = 0.57, P < 0.001) but not with any indices of abdominal fat distribution. After weight loss the associations became significant for hip and waist circumference as well as for visceral and abdominal subcutaneous fat. Changes in leptin correlated with changes in all indices of obesity except visceral fat. CONCLUSIONS: Plasma leptin concentrations reflect not only total fat mass but also adipose tissue distribution, especially peripheral fat. Plasma leptin values per kilogram of fat mass do not change significantly with modest weight loss.     

Relationship between plasma leptin levels and the tumor necrosis factor-alpha system in obese subjects.

OBJECTIVE: To evaluate the relationship between plasma leptin and the tumor necrosis factor-alpha (TNFalpha), TNF receptor p60 (TNF-R1) and TNF receptor p80 (TNF-R2) concentrations in obese subjects. DESIGN: Case-control study. SETTING: Outpatient's Service for Prevention and Treatment of Obesity at the University Hospital. MEASUREMENTS: Body mass index (BMI), waist circumference, hip circumference, waist-to-hip ratio (WHR), fasting plasma glucose, fasting plasma insulin, homeostasis model assessment of insulin resistance (HOMA IR), plasma leptin, TNFalpha, TNF-R1 and TNF-R2 concentrations were evaluated in obese subjects (n = 42) and in age- and gender-matched, lean healthy controls (n = 16). RESULTS: In obese subjects, fasting plasma glucose and insulin, HOMA IR, plasma leptin, TNFalpha, TNF-R1 and TNF-R2 concentrations were significantly higher than in controls. Furthermore, females showed higher leptin, TNF-R1 and TNF-R2 plasma concentrations compared to males, in both control and obese subjects. In control subjects, plasma leptin concentrations showed a direct correlation with BMI (r=0.74, P<0.001), hip circumference (r=0.94, P<0.001), TNF-R1 (r=0.79, P<0.001) and TNF-R2 (r=0.64, P<0.01), and a negative correlation with WHR (r=-0.58, P<0.05). In obese subjects, we found a direct correlation between plasma leptin concentrations and BMI (r=0.67, P<0.001), hip circumference (r=0.66, P<0.001), fasting glucose (r=0.37, P<0.05), fasting insulin (r=0.31, P<0.05), HOMA IR (r=0.38, P<0.05), TNF-R1 (r=0.71, P<0.001) and TNR-R2 (r=0.66, P<0.001), while a negative correlation was found between circulating leptin and WHR (r=-0.44, P<0.01). In multivariate analysis, plasma leptin concentrations were significantly associated with BMI (P=0.015) and gender (P=0.047) in the control group, while in obese subjects, plasma leptin showed a significant association with BMI (P=0.019) and TNF-R1 (P=0.012). CONCLUSIONS: Our results are consistent with the hypothesis that the TNFalpha system could be involved in the regulation of plasma leptin concentrations in obese subjects.     

Leptin and bone mineral density: a cross-sectional study in obese and nonobese men

Leptin has been suggested to decrease bone mineral density (BMD). This observational analysis explored the relationship between serum leptin and BMD in 327 nonobese men (controls) (body mass index 26.1 +/- 3.7 kg/m(2), age 49.9 +/- 6.0 yr) and 285 juvenile obese men (body mass index 35.9 +/- 5.9 kg/m(2), age 47.5 +/- 5.1 yr). Whole-body dual-energy x-ray absorptiometry scan measured BMD, fat mass, and lean mass. Fasting serum leptin (nanograms per milliliter) was strongly associated with fat mass (kilograms) in both controls (r = 0.876; P < 0.01) and juvenile obese (r = 0.838; P < 0.001). An inverse relation between BMD adjusted for body weight and serum leptin emerged in both the control group (r = -0.186; P < 0.01) and the juvenile obese group (r = -0.135; P < 0.05). In a multiple linear regression, fat mass, lean body mass, and occupational physical activity were positively associated with BMD in the control group, whereas in the juvenile obese, only lean body mass was positively associated with BMD and smoking negatively associated with BMD. Our study supports that leptin is inversely associated with BMD and may play a direct role in the bone metabolism in nonobese and obese Danish males, but it also stresses the fact that the strong covariation between the examined variables is a shortcoming of the cross-sectional design.     

Effects of obstructive sleep apnea syndrome on serum aminotransferase levels in obese patients

PURPOSE: Obesity has been associated with obstructive sleep apnea and hepatic steatosis. We investigated the effects of obstructive sleep apnea and treatment with nasal continuous positive airway pressure (CPAP) on serum aminotransferase levels in obese patients. METHODS: We studied 40 obese men with obstructive sleep apnea syndrome. None had hepatitis B antigen or C antibody, autoimmune disease, or an excessive intake of alcohol. Serum levels of aspartate aminotransferase, alanine aminotransferase, triglyceride, glucose, insulin, and leptin were determined in the afternoon and in the morning immediately after sleep, before and after nasal CPAP treatment. RESULTS: Aminotransferase levels were abnormal in 35% (n = 14) of patients. Before treatment, mean (+/- SD) aspartate aminotransferase levels were higher in the morning than in the previous afternoon (presleep, 34 +/- 20 IU/L; postsleep, 39 +/- 28 IU/L; P = 0.006). The overnight mean increases in aminotransferase levels were less marked after the first night of nasal CPAP treatment (aspartate aminotransferase: from 6 +/- 11 IU/L to 2 +/- 6 IU/L, P = 0.0003; alanine aminotransferase: from 5 +/- 9 IU/L to 2 +/- 6 IU/L, P = 0.006). Leptin levels (n = 23) decreased significantly after treatment (P = 0.0002), whereas insulin resistance (calculated by the homeostasis model assessment method) and triglyceride levels were unchanged. Improvements in aspartate and alanine aminotransferase levels were maintained after 1 and 6 months of nasal CPAP treatment. CONCLUSION: Nasal CPAP therapy may have beneficial effects on serum aminotransferase abnormalities in obese patients who have obstructive sleep apnea.