老年阻塞性睡眠呼吸暂停综合征与高血压及胰岛素抵抗的相关性研究

目的探讨阻塞性睡眠呼吸暂停综合征(OSAS)与高血压及胰岛素抵抗(IR)的关系。方法随机选择符合OSAS患者48例作为OSAS组,并分为高血压组(28例)和正常血压组(20例)2个亚组,同期选择无OSAS的高血压患者30例作为单纯高血压组,健康体检者26例作为正常对照组,均进行整夜睡眠呼吸监测(7 h),并记录睡眠呼吸暂停低通气指数(AHI)等;空腹血糖(FPG)及空腹胰岛素(FINS)测定,对患者进行24 h的动态血压监测并进行相关分析。结果与单纯高血压组比较,高血压组患者非杓形血压比例和脉压均明显升高,差异有统计学意义(P0.05,P0.01)。OSAS组患者的FPG、FINS水平及胰岛素抵抗指数(HOMA-IR)均明显高于正常对照组,差异有统计学意义(P0.05);OSAS患者的AHI与FINS和HOMA-IR均呈正相关。结论 OSAS与IR存在独立的相关性,可能通过IR导致并进一步加重心血管疾病的发生和发展。     

老年慢性阻塞性肺疾病患者血浆脂联素的水平

目的 分析老年慢性阻塞性肺疾病(COPD)患者血浆脂联素水平与C反应蛋白(CRP)、空腹血糖(FPG)、胰岛素抵抗(IR)及肥胖指标的关系.方法 选择住院的老年COPD患者60例,按病程分为急性加重期和临床稳定期,在不同时期测定血浆脂联素、CRP、FPG、胰岛素(FINS)、体重指数(BMI)、胰岛素抵抗指数(HOMA-IR).选择同期健康老年人50例作为对照.结果 COPD急性加重期及临床稳定期血浆脂联素均较对照组显著升高(P<0.01),临床稳定期血浆脂联素较急性加重期进一步升高(P<0.01);COPD急性加重期CRP、FPG、FINS、HOMA-IR显著高于临床稳定期及对照组(P<0.01);COPD临床稳定期FINS、HOMA-IR显著高于对照组(P<0.05);急性加重期脂联素与CRP、FPG、FINS、HOMA-IR、BMI均呈显著负相关(P<0.05或P<0.01).结论 老年COPD患者血浆脂联素水平升高并伴一定的胰岛素抵抗,脂联素在COPD稳定期进一步抬高,脂联素与CRP、FPG、IR及肥胖指标存在一定的相关性.     

老年代谢综合征血清Adiponectin,Resistin与IR的相关性研究

90患者分为MS合并T2DM组、肥胖合并T2DM组、单纯肥胖组,健康对照组各30例。结果肥胖各组血清抵抗素、胰岛素抵抗指数(HOMA-IR)均高于对照组(P0.01),血清脂联素水平均低于对照组(P0.01)。多元线性逐步回归分析显示,体质量指数(BMI)、FPG、脂联素、抵抗素是影响老年MS患者IR的独立危险因素。结论老年MS患者在疾病各个时期均存在IR,脂联素、抵抗素可影响老年MS患者IR的程度。     

痛风患者脂联素水平及胰岛素抵抗与动脉粥样硬化的关系

目的通过研究痛风患者颈动脉内膜-中膜厚度(IMT)与脂联素、胰岛素抵抗(IR)的关系,探讨脂联素、IR在痛风患者动脉粥样硬化中的作用。方法测定60例痛风患者、40例尿酸正常的健康志愿者(对照组)空腹血糖(FPG)、空腹胰岛素(FINS)、甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白(HDL-C)、低密度脂蛋白(LDL-C)、血尿酸(Ua)及脂联素(APN)水平,测量颈动脉内膜-中膜厚度(IMT),同时计算体重指数(BMI)、胰岛素抵抗指数(HOMA-IR);并以颈动脉IMT为应变量,FPG、FINS、血脂、BMI、HOMA-IR、Ua、脂联素为自变量,进行多元逐步回归分析。结果痛风组TC、LDL-C、FINS、Ua、HOMA-IR高于对照组(P0.05或P0.01),且颈动脉IMT高于对照组(P0.05),而脂联素水平则较对照组明显降低(P0.05)。多元逐步回归分析显示,脂联素、LDL-C和BMI是影响痛风患者动脉粥样硬化的独立危险因素。结论痛风患者较尿酸正常的人群存在明显的代谢紊乱和IR,且血清脂联素水平降低,更容易发生动脉粥样硬化。     

阻塞性睡眠呼吸暂停低通气综合征患者血清脂肪细胞因子变化及其临床意义

目的探讨阻塞性睡眠呼吸暂停低通气综合征（OSAHS）患者血清脂联素、抵抗素变化及其临床意义。方法选择年龄、BMI匹配的OSAHS患者90例（OSAHS组）和单纯肥胖者33例（对照组）;根据呼吸暂停低通气指数（AHI）将OSAHS组分为轻度组、中度组和重度组,并检测各组血清脂联素、抵抗素、血压、空腹血糖（FPG）、胰岛素（FINS）、血脂,以及AHI、最低血氧饱和度（SaO2）。结果与对照组比较,OSAHS组抵抗素、AHI、FINS明显升高,脂联素、最低SaO2明显降低（P〈0.05或〈0.01）;轻度组、中度组和重度组间脂联素、抵抗素比较有统计学差异（P均〈0.05）。OSAHS患者血清脂联素水平与血压、BMI、FPG、AHI呈负相关,与最低SaO2呈正相关（P〈0.01或〈0.05）;抵抗素水平与BMI、FINS、AHI呈正相关,与最低SaO2呈负相关（P〈0.01或〈0.05）。结论 OSAHS患者血清脂联素降低、抵抗素升高,其水平与OSAHS病情严重程度相关,是导致OASHS发生、发展的重要因素。     

普罗布考对阻塞性睡眠呼吸暂停低通气综合征患者的影响研究

目的探讨普罗布考对阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者的影响。方法选取2013年12月—2014年12月唐山市人民医院收治的OSAHS患者88例,采用随机数字表法分为对照组和观察组,每组44例。对照组患者给予阿托伐他汀钙片治疗,观察组患者给予普罗布考治疗;两组患者均连续治疗12个月。比较两组患者治疗前后血脂指标[包括总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)]、空腹血糖、空腹胰岛素、胰岛素抵抗指数(HOMA-IR)、睡眠呼吸暂停低通气指数(AHI)、最低血氧饱和度(LSaO_2)及血清抵抗素、脂联素水平,AHI与OSAHS患者其他观察指标间的相关性分析采用Pearson相关性分析。结果两组患者治疗前TC、TG、LDL-C、HDL-C比较,差异无统计学意义(P0.05);治疗后观察组患者TC、TG、LDL-C低于对照组,HDL-C高于对照组(P0.05)。两组患者治疗后TC、TG、LDL-C低于治疗前,HDL-C高于治疗前(P0.05)。两组患者治疗前空腹血糖、空腹胰岛素、HOMA-IR及治疗后空腹血糖比较,差异无统计学意义(P0.05);治疗后观察组患者空腹胰岛素、HOMA-IR低于对照组(P0.05)。两组患者治疗后空腹胰岛素、HOMA-IR低于治疗前(P0.05)。两组患者治疗前AHI、LSaO_2比较,差异无统计学意义(P0.05);治疗后观察组患者AHI低于对照组,LSaO_2高于对照组(P0.05)。两组患者治疗后AHI低于治疗前,LSaO_2高于治疗前(P0.05)。两组患者治疗前血清抵抗素、脂联素水平比较,差异无统计学意义(P0.05);治疗后观察组患者血清抵抗素水平低于对照组,血清脂联素水平高于对照组(P0.05)。两组患者治疗后血清抵抗素水平低于治疗前,血清脂联素水平高于治疗前(P0.05)。Pearson相关性分析结果显示,AHI与OSAHS患者TC、TG、LDL-C、空腹胰岛素、HOMA-IR及血清抵抗素水平呈正相关(r值分别为0.536、0.392、0.497、0.386、0.401、0.512,P0.05),与OSAHS患者HDL-C、LSaO_2及血清脂联素水平呈负相关(r值分别为-0.415、-0.608、-0.473,P0.05)。结论普罗布考能有效改善OSAHS患者血脂代谢、糖代谢及氧合状态;AHI与OSAHS患者血清抵抗素水平呈正相关,与OSAHS患者血清脂联素水平呈负相关。     

2型糖尿病家系血清脂联素和抵抗素的表达及其与胰岛素抵抗的相关性

目的探讨2型糖尿病（T2DM）家系正常糖耐量一级亲属（一级亲属）血清脂联素和抵抗素表达水平的变化,研究脂联素和抵抗素与胰岛素抵抗（IR）的相关性。方法收集广西壮族地区T2DM家系45个,在排除糖尿病和糖耐量损害的前提下,选择一级亲属为一级亲属组（83例）,先证者的配偶或其同胞的配偶为对照组（76例）,检测所有受试者的空腹血糖（FPC）、空腹胰岛素（FINS）、胰岛素原（FPI）、血脂、脂联素和抵抗素水平。采用稳态模型法（HOMA）计算胰岛素抵抗指数（HOMA—IR）。结果一级亲属组的甘油三酯（TG）、FPI、FINS、HOMA-IR和抵抗素水平显著高于对照组（P〈0．05或P〈0．01）,高密度脂蛋白（HDL）和脂联素显著低于对照组（P〈0．05）。多元线性逐步回归分析显示,FPG、体质指数（BMI）、脂联素、抵抗素是影响T2DM家系一级亲属胰岛素抵抗的独立危险因素。结论T2DM家系一级亲属在未发生糖尿病时已存在胰岛素抵抗,脂联素、抵抗素可影响T2DM家系一级亲属IR的程度。     

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。     

巴马小型猪 T2DM 模型胰岛素抵抗及瘦素、抵抗素水平的变化

目的探讨巴马小型猪2型糖尿病(T2DM)模型胰岛素抵抗(IR)及瘦素、抵抗素水平的变化。方法选用健康雄性巴马小型猪10只,随机分为两组各5只。对照组喂养普通饲料;模型组喂养高脂高糖饲料,共喂养10个月。11个月初模型组腹腔注射链脲佐菌素(STZ)100 mg/kg,1周后重复1次;对照组腹腔注射等剂量柠檬酸—柠檬酸钠缓冲液,12个月末试验结束。检测两组空腹血糖(FPG)、空腹胰岛素(FINS)及血清瘦素、抵抗素水平,同时采用HOMA模型公式计算胰岛素抵抗指数(HOMA-IR)。结果与对照组比较,高脂高糖饲料喂养10个月模型组小型猪体质量、FPG、FINS及HOMA-IR升高(P均<0.01);与对照组相比,模型组STZ给药后(12个月末试验结束时)FPG进一步升高,FINS水平明显下降(P均<0.01);与对照组比较,模型组血清瘦素、抵抗素水平升高(P均<0.05),且HOMA-IR与瘦素、抵抗素呈正相关(r分别为0.893、0.933,P均<0.05)。结论 T2DM小型猪血清瘦素、抵抗素水平升高,与HOMA-IR密切相关。     

妊娠期糖尿病患者脂肪组织脂联素mRNA表达与胰岛素抵抗的关系

目的 探讨妊娠期糖尿病（GDM）患者脂肪组织脂联素mRNA表达与胰岛素抵抗（IR）的关系.方法 检测GDM患者（GDM组） 的皮下与网膜脂肪脂联素mRNA、血脂、空腹胰岛素（FINS）、游离脂肪酸（FFA）及胰岛素抵抗指数（HOMA-IR）等,并与正常孕妇（NGT组）和非育龄择期手术者（对照组）进行比较.结果 GDM组、NGT组和对照组的皮下脂肪脂联素mRNA表达均高于其网膜脂肪水平;对照组、NGT组、GDM组皮下、网膜脂肪脂联素mRNA表达依次降低（P均＜0.01）.三组TG、LDL-C、FFA、FINS 和HOMA-IR比较均有统计学差异（P均＜0.01）.GDM组网膜脂肪脂联素mRNA表达与CRP、FPG、FINS、HOMA-IR和孕前BMI等呈负相关（P＜0.01或＜0.05）.结论 GDM患者的网膜脂肪脂联素mRNA表达降低与其IR及GDM发生有关.     

Adiponectin in patients with obstructive sleep apnea syndrome: course and physiological relevance

BACKGROUND: Adiponectin is an adipocyte-derived hormone with anti-inflammatory and insulin-sensitizing properties. Insulin resistance is a typical feature of the obstructive sleep apnea syndrome (OSAS). OBJECTIVES: Since nasal continuous positive airway pressure (nCPAP) treatment improves insulin sensitivity in patients with OSAS, we investigated serum adiponectin levels before and during nCPAP treatment to clarify possible interactions between the adiponectin levels and insulin sensitivity in patients with OSAS. METHODS: Thirty nondiabetic, obese patients with OSAS (mean age 56.4 +/- 11.1 years; apnoea-hypopnoea index (AHI) 46.03 +/- 19.57) underwent CPAP treatment. Adiponectin levels and the levels of proinflammatory cytokines and proteins reflecting platelet activation [regulated on activation normally T cell expressed and secreted (RANTES) and soluble P-selectin (sCD62p)], as well as the insulin sensitivity index were measured before, and after 2 days and 3 months of CPAP treatment. RESULTS: Insulin sensitivity increased significantly under nCPAP treatment, whereas adiponectin levels decreased after 2 days of nCPAP treatment, but returned to baseline levels after 3 months of nCPAP treatment. The increase in insulin sensitivity was more pronounced in patients with the highest adiponectin levels at baseline (p = 0.021) after adjustment for body fat (p = 0.003). During treatment, changes in adiponectin levels were highly predictable by the insulin sensitivity index. CONCLUSIONS: We found a significant relation between adiponectin and the insulin sensitivity index in overweight patients with OSAS. The lack of a long-lasting change in adiponectin may be explained by the overwhelming influence of the body mass index on adiponectin secretion, which was unchanged during nCPAP treatment.     

瘦素与妊娠糖尿病患者胰岛素抵抗及胎儿发育的相关性

目的 探讨瘦素及可溶性瘦素受体(sLR)在妊娠糖尿病发病及胎儿发育中的作用.方法 选取2014年1月至12月在厦门大学附属成功医院连续产检并分娩的673名孕妇为研究对象,跟踪随访至孕晚期.根据糖耐量试验结果,采用随机抽样法选取50例血糖控制良好的妊娠糖尿病患者纳入妊娠糖尿病组,根据一般资料进行匹配选取50名糖耐量试验结果阴性者纳入正常妊娠组.根据妊娠周数分为孕早期和孕晚期亚组,比较两组不同孕期血清及脐血瘦素、sLR、脂联素、抵抗素及生化指标水平,计算稳态模型评估-胰岛素抵抗指数(HOMA-IR),精确测量新生儿生长发育指标,使用多元Logistic回归分析孕早期胰岛素抵抗的危险因素,同时采用Spearman相关性分析血清瘦素与sLR、脂联素、抵抗素及生化指标水平的相关性.结果 与正常妊娠组相比,妊娠糖尿病组孕早期血清瘦素、甘油三酯、总胆固醇、低密度脂蛋白-胆固醇(LDL-C)、空腹胰岛素(FINS)、HOMA-IR明显升高(t=0.938～6.864,P均＜0.05),sLR、脂联素显著降低(t=9.237、2.216,P均＜0.05),抵抗素、高密度脂蛋白-胆固醇(HDL-C)、空腹血糖差异无统计学意义(P均＞0.05).与正常妊娠组相比,妊娠糖尿病组孕晚期血清瘦素、抵抗素、空腹血糖、FINS、甘油三酯、总胆固醇、LDL-C、HOMA-IR明显升高(t=0.429 ～ 13.787,P均＜0.05),sLR、脂联素显著降低(t=2.216、5.623,P均＜0.05),HDL-C差异无统计学意义(P＞0.05).与正常妊娠组相比,妊娠糖尿病组脐血瘦素、抵抗素明显升高(t=1.007、11.857,P均＜0.05),sLR、脂联素显著降低(t=0.201、4.558,P均＜0.05).多元Logistic回归分析显示,瘦素(OR =1.288,95％ CI:1.137 ～4.370)、抵抗素(OR=1.223,95％CI:1.035～ 1.570)、总胆固醇(OR=1.216,95％CI:1.026 ～1.823)、甘油三酯(OR=1.357,95％CI:1.008～ 3.572)、LDL-C (OR=1.634,95％ CI:1.251～3.764)是妊娠糖尿病组孕早期发生胰岛素抵抗的独立危险因素,sLR (OR =0.714,95％ CI:0.161～0.893)、脂联素(OR =0.352,95％CI:0.112 ～0.510)是妊娠糖尿病组孕早期发生胰岛素抵抗的保护性因素.妊娠糖尿病组孕晚期母体血瘦素含量与sLR、脂联素均呈负相关(r=-0.16、-1.13,P均=0.000),与抵抗素呈正相关(r=0.269,P=0.019).妊娠糖尿病组脐血瘦素含量与sLR、脂联素均呈负相关(r=-0.147、-1.250,P均=0.000),与抵抗素、体重、Ponderal 指数均呈正相关(r =0.410、0.673、0.301,P均＜0.05),与头围、身长无关(P均＞0.05).结论 瘦素及sLR与妊娠糖尿病患者胰岛素抵抗存在相关性,但与胎儿宫内生长和发育无关.     

Obstructive sleep apnoea syndrome, plasma adiponectin levels, and insulin resistance

OBJECTIVE: To investigate whether sleep-disordered breathing and/or plasma adiponectin levels are associated with insulin resistance independent of obesity or fat distribution in obstructive sleep apnoea syndrome (OSAS). DESIGN: Cross-sectional clinical study. PATIENTS: Two-hundred and thirteen Japanese patients with OSAS aged 27-80 years were divided into three groups: 30 with mild OSAS [apnoea-hypopnoea index (AHI) = 10.3 +/- 0.9 episodes/h, minimum oxygen saturation (min SpO2) = 87.3 +/- 0.9%], 98 with moderate OSAS (AHI = 28.9 +/- 0.6 episodes/h, min SpO2 = 82.1 +/- 0.7%), and 85 with severe OSAS (AHI = 68.1 +/- 2.8 episodes/h, min SpO2 = 72.3 +/- 1.6%). Twenty-one patients undergoing diabetic treatments (two mild, nine moderate and 10 severe) were excluded from the assessment of insulin resistance and plasma adiponectin measurements. MEASUREMENTS: Fat distribution [evaluated according to visceral (V) and subcutaneous (S) fat areas using computed tomography scanning at the umbilical level], blood pressure, metabolic parameters and hormones including insulin and adiponectin were measured. After full polysomnography, venous blood was collected between 0600 and 0700 h. RESULTS: Severe OSAS patients were more hypertensive than mild and moderate OSAS. Fasting plasma glucose (FPG) and fasting plasma insulin and homeostasis model assessment of insulin resistance (HOMA-IR) levels were all higher in severe OSAS than mild and moderate OSAS patients. HOMA-IR was correlated not only with obesity [body mass index (BMI), V and S areas] but also with apnoea (AHI, min SpO2 and desaturation time). Additionally, HOMA-IR was correlated positively with haemoglobin (Hb)A1c, systolic (SBP) and diastolic blood pressure (DBP), triglycerides and free fatty acids (FFA), and negatively with high density lipoprotein (HDL)-cholesterol, suggesting that insulin resistance is a key component of the metabolic syndrome in OSAS. Plasma adiponectin levels were not different between mild, moderate and severe OSAS groups. Plasma adiponectin levels were correlated with HOMA-IR and V area, but not AHI or min SpO2. Stepwise multiple regression analysis, however, revealed that BMI, AHI and plasma adiponectin were independently associated with HOMA-IR. CONCLUSION: Sleep-disordered breathing was associated with insulin resistance independent of obesity. Although plasma adiponectin was also an independent determinant of HOMA-IR in OSAS patients, plasma adiponectin was more closely related to obesity than to sleep apnoea. Although treatment of sleep-disordered breathing with nasal continuous positive airway pressure reportedly improves insulin sensitivity, our findings suggest that treatment of obesity is also essential in ameliorating insulin resistance at least through increased plasma adiponectin levels in OSAS.     

Serum concentrations of adipocytokines in patients with hyperthyroidism and hypothyroidism before and after control of thyroid function

OBJECTIVE: Adipose tissue is a hormonally active system that produces and releases different bioactive substances. Leptin, adiponectin and resistin are some of the recently discovered adipocytokines that participate in the regulation of intermediate metabolism. The aim of this study was to evaluate the circulating levels of leptin, adiponectin and resistin in patients with thyroid dysfunction before and after normalization of thyroid function with appropriate therapy. PATIENTS AND MEASUREMENTS: We studied 20 patients with hyperthyroidism (16 women and 4 men; mean age 47.2 +/- 3.9 years) and 20 patients with hypothyroidism (17 women and 3 men; 51.5 +/- 4.1 years). A group of 20 euthyroid subjects served as control group. Patients were evaluated at the time of diagnosis and again after normalization of thyroid function with appropriate therapy. Serum concentrations of free T4 (FT4), total T3, TSH, insulin, leptin, adiponectin and resistin were measured in all subjects. RESULTS: Hyperthyroid patients showed significantly decreased leptin levels in comparison with controls (11.0 +/- 1.1 vs. 30.4 +/- 5.0 microg/l, P < 0.001). No significant differences in adiponectin levels between hyperthyroid and control groups were found (27.8 +/- 4.0 vs. 46.0 +/- 12.0 mg/l, NS). Patients with hyperthyroidism exhibited reduced resistin levels in comparison with euthyroid subjects (6.4 +/- 0.8 vs. 8.4 +/- 0.7 microg/l, P < 0.05). Normalization of circulating thyroid hormone was accompanied by a nonsignificant increase in leptin levels (12.9 +/- 1.7 microg/l, P < 0.01 vs. control) and no significant modification both in adiponectin (32.0 +/- 7.1 mg/l, NS) and resistin (5.4 +/- 0.7 microg/l, NS) levels. Adjustment of adipocytokine concentrations for body mass index (BMI) showed that treatment of hyperthyroidism induced a significant reduction in adjusted resistin concentrations (0.21 +/- 0.03 vs. 0.28 +/- 0.03 microg/l/BMI units, P < 0.05), with no changes in adjusted leptin and adiponectin. Hypothyroid patients showed significantly lower leptin levels compared with the controls (16.0 +/- 3.5 vs. 30.4 +/- 5.0 microg/l, P < 0.05). Adiponectin levels in patients with hypothyroidism (71.8 +/- 16.0 mg/l) were similar to those in the control group and were not modified with therapy. Resistin levels were significantly reduced among hypothyroid patients (5.8 +/- 1.0 microg/l, P < 0.05), and were not increased after levothyroxine therapy. A significant rise in BMI-corrected leptin levels was observed after replacement therapy, with no changes in adiponectin- and resistin-corrected values. CONCLUSIONS: The results suggest that (1) low serum leptin levels are present in both hyperthyroid and hypothyroid patients but are only increased after therapy in the latter; (2) resistin might be implicated in the insulin resistance state that accompanies thyrotoxicosis; and (3) inadequate secretion of adiponectin seems to have no role in metabolic changes associated with thyroid dysfunction.     

Elevated plasma resistin concentrations in patients with liver cirrhosis

Background: Resistin, an adipose‐derived polypeptide hormone, has been proposed to be a candidate in insulin resistance, although its role in humans remains controversial. Liver cirrhosis (LC) is characterized by an elevated number of circulating proinflammatory cytokines, hyperinsulinemia and insulin resistance. The aim of this study was to determine the plasma resistin levels in patients with LC. Methods: Resistin levels were determined in 79 patients with LC and in 31 healthy controls. Patients included 34 with Child–Pugh grade A, 30 with Child's B and 15 with Child's C LC. Fasting plasma glucose, fasting plasma insulin, adiponectin, the homeostatic model assessment insulin resistance (HOMA‐IR) index, quantitative insulin sensitivity check index (QUICKI) and biochemical parameters were also determined. Results: Plasma resistin levels were 7.61 ± 6.70 ng/mL in the LC patients and 3.38 ± 1.68 ng/mL in the controls, respectively. The plasma resistin levels were significantly elevated in patients with LC in comparison to the controls (P < 0.01). The plasma resistin levels increased in a stepwise fashion in line with a higher grade according to Child–Pugh classification. Fasting plasma insulin, adiponectin and HOMA‐IR index were also significantly elevated in patients with LC in comparison to controls. Inversely, QUICKI significantly decreased in patients with LC. According to Spearman's rank correlation, log resistin showed significantly positive correlation with fasting plasma insulin, log adiponectin, HOMA‐IR index, and a negative correlation with QUICKI (P < 0.01). The plasma resistin levels did not correlate with sex, body mass index and fasting plasma glucose levels. Conclusion: The plasma resistin levels increased in patients with LC, thus showing a positive correlation with fasting plasma insulin, adiponectin, HOMA‐IR index, and a negative correlation with QUICKI. Although a decreased extraction of resistin due to reduced liver function cannot be ruled out, resistin may contribute to insulin resistance in patients with LC. The pathophysiological roles of resistin in LC still require further investigation.     

Adipokine levels in Cushing's syndrome; elevated resistin levels in female patients with Cushing's syndrome

BACKGROUND: Cushing's syndrome (CS) is associated with central adiposity, insulin resistance and impaired glucose homeostasis. Adipose tissue is thought to regulates glucose homeostasis via circulating adipokines, such as resistin, leptin and adiponectin, although their role in the insulin resistance associated with CS has not been established. DESIGN: We examined the relationship between insulin resistance and adipokine levels in CS patients. We compared plasma levels of resistin, leptin and adiponectin in 10 women and four men patients with CS, with 14 health subjects matched for age, gender and body mass index. A subgroup of three women and four men with pituitary-dependent CS were re-examined at least 9 months after curative surgery. RESULTS: CS patients had significantly more truncal fat and less lean body mass as assessed by DEXA compared to control subjects. Total cholesterol, triglycerides and insulin resistance, as calculated using the homeostasis model assessment of insulin resistance (HOMA-R), was significantly increased in CS patients. Of the adipokines measured, only resistin was significantly different between female CS patients and female control subjects (5.05 +/- 0.56 vs. 2.91 +/- 0.39 micro g/l, P = 0.015). Curative surgery significantly reduced total body fat and truncal fat, leptin, total and low-density lipoprotein (LDL) cholesterol, glucose and HOMA-R. A reduction in both resistin and adiponectin was also observed but the differences between pre- and post-treatment levels did not achieve statistical significance. CONCLUSION: Here we report for the first time that resistin levels are significantly elevated in CS patients and may be important in the insulin resistance associated with glucocorticoid excess.     

The effects of rosiglitazone and metformin on the plasma concentrations of resistin in patients with type 2 diabetes mellitus

Resistin is a protein secreted from adipose tissue that is thought to play a role in insulin sensitivity. We examined the effects of rosiglitazone and metformin on the plasma resistin levels in individuals with type 2 diabetes mellitus. Patients with type 2 diabetes mellitus who showed poor glycemic control with glimepiride (4 mg/d) were randomized to rosiglitazone (4 mg/d) and metformin (500 mg bid) treatment groups. All subjects continued glimepiride treatment as well. The plasma concentrations of resistin were measured at baseline and at 6 months of treatment for both groups. The anthropometric parameters, fasting plasma glucose, HbA1c, total cholesterol, triglyceride, high-density lipoprotein cholesterol, free fatty acids, and adiponectin concentrations were also measured. After 6 months of treatment, the reduction in plasma glucose levels was similar between the 2 groups. There were no significant changes in the lipid profiles of either group during the study period. The plasma resistin levels decreased in the rosiglitazone group (2.49 +/- 1.93 vs 1.95 +/- 1.59 ng/ml; P < .05) but increased in the metformin group (2.61 +/- 1.69 vs 5.13 +/- 2.81 ng/ml; P < .05). The plasma adiponectin concentrations were increased in the rosiglitazone group (2.91 +/- 1.46 vs 4.23 +/- 1.77 microg/ml; P < .05) but were unchanged in the metformin group. In summary, rosiglitazone treatment decreased the plasma resistin levels whereas metformin treatment increased them in patients with type 2 diabetes mellitus showing poor glycemic control with sulfonylurea therapy. These results suggest that the observed changes in plasma resistin levels are not the consequences of improved insulin resistance, nor are they consequences of glycemic control. Considering the potential role of resistin in insulin resistance, decrease in resistin levels may contribute to improving insulin action with rosiglitazone treatment.     

Increased serum resistin in adults with prader-willi syndrome is related to obesity and not to insulin resistance

CONTEXT: Determinants of insulin resistance in Prader-Willi syndrome (PWS) are not completely understood. The discovery of several adipokines with relevant effects on insulin resistance and cardiovascular complications of metabolic syndrome offered new tools of investigation of insulin resistance in PWS. OBJECTIVE: The purpose of this study was to measure serum resistin and mRNA in adipose tissue of patients with PWS, those with simple obesity, and healthy controls and correlate resistin levels with anthropometric and biochemical features. DESIGN: Twenty-eight adult PWS patients, 29 obese patients, and 25 healthy controls were studied. Anthropometric variables were measured and fasting serum and plasma were collected for measurement of resistin, adiponectin, leptin, lipid profile, glucose, and insulin. RESULTS: Serum resistin and resistin mRNA expression in adipose tissue was significantly higher in PWS patients, compared with both healthy lean controls and obese patients. Moreover, on regression analysis resistin was significantly correlated with body mass index, whereas no significant association was found between resistin and homeostasis model assessment index. A weak association between resistin and adiponectin was found in the PWS group only. However, on multivariate analysis only the correlation between resistin and body mass index remained significant. CONCLUSIONS: These results support a link between circulating resistin and obesity in humans but do not support a role for resistin in human insulin resistance.