2型糖尿病一级亲属脂联素等与胰岛素抵抗的相关研究

测定糖耐量正常T2DM患者一级亲属35例，及对照组42例的脂联素、抵抗素、TNF-α。结果1．一级亲属组脂联素水平低于正常对照组（12．29±3．64mg／L vs 14．66±3．43mg／L，P〈0．05），而抵抗素、TNF-α水平显著高于正常组（分别是19．02±6．85Pg／ml vs 15．68±6．24pg／ml，P〈0．05；14．12±2．87pg／ml vs 10．43±2．58pg／ml，P〈0．05）；2．一级亲属组IR指数与脂联素呈负相关（r=-0．53，P〈0．05），与抵抗素、TNF-α呈正相关（分别为r=0．62，P〈0．05；r=0．48，P〈0．05）。结论脂联素、抵抗素、TNF-α可能与T2DM患者一级亲属的IR相关。     

单一性低促性腺激素型性腺功能减退症患者血清脂联素与睾酮水平的关系

目的观察对单一性低促性腺激素型性腺功能减退症（IHH）患者脂联素与睾酮水平的关系。方法通过分析临床资料及激素测定、促性腺激素释放激素激发试验确诊IHH，检测23例IHH患者和15名正常男性血清脂联素和睾酮水平。结果与体重指数、腰臀比以及血压均匹配的正常对照组相比，IHH患者睾酮水平显著低于正常[（0．23±0．18 vs 4．20±1．90）μg／L，P〈0．01]，其脂联素水平显著升高[（11．3±1．8vs8．7±1．2）mg／L，P〈0．01]。对两组进行相关分析显示，血清脂联素水平与睾酮水平呈负相关（r=-0．570，P〈0．01）。结论IHH低睾酮水平人群中脂联素水平显著升高，提示脂联素与睾酮水平之间存在密切关系。     

脂肪组织瘦素基因与非酒精性脂肪肝的研究

目的探讨非酒精性脂肪肝(NAFLD)患者脂肪组织瘦素mRNA基因表达水平和胰岛素抵抗与血浆瘦素等的相关性。方法行熳性胆囊炎、胃溃疡、腹股沟疝等择期手术的NAFLD患者21例、对照组患者24例,于术中取少许腹部皮下和网膜脂肪组织送检。应用SYBR Green I实时定量逆转录聚台酶链反应法检测瘦素mRNA的表达水平,用稳态模型法计算胰岛素抵抗指数,用酶联免疫吸附法测定血浆瘦素和胰岛素水平。结果NAFLD和对照组瘦素基因表达值分别为1．32±0．12、0．99±0．05,1．10±0．09、0．87±0．13；瘦素基因表达和胰岛素抵抗指数与血浆瘦素浓度直接关联(r值分别为0．72、0．69,P值均＜0．05)。结论脂肪组织瘦素基因高表达是高瘦素血症的主要原因,肥胖和非肥胖的NAFLD患者存在瘦素抵抗和胰岛素抵抗,提示瘦素抵抗与胰岛素抵抗一样和NAFLD发病密切相关。     

氯通道CIC-1、CIC-2在人心房肌的表达及与心房颤动的关系

目的研究氯通道CIC-1和CIC-2基因在人心房组织的表达及与心房颤动（AF）的关系。方法将71例风湿性心瓣膜病接受换瓣手术患者分为三组，窦性心律（SR）组31例，阵发性房颤（PAF）组7例，慢性房颤（CAF）组33例，于术中获取右心耳组织，应用半定量逆转录-聚合酶链反应（RT—PCR）检测心房组织CIC-1和CIC-2的mR—NA相对含量。结果（1）CIC—1、CIC-2基因在人心房组织有表达。②与SR组比较，PAF组CIC-1的mRNA表达增加但无统计学意义（1．05±0．22vs1．01±0．13，P〉0．05），CAF组的表达明显增加（1．25±0．18vs1．01±0．13，P〈0．001），CAF组较PAF组亦明显增加（P〈0．01）。CIC-1的mRNA表达水平与左房内径、AF持续时间呈正相关[（r=0．344，P=0．003）（r=0．405，P〈0．001）]。③与SR组比较，PAF组CIC-2的mRNA表达无增加（1．03±0．14vs1．04±0．15，P〉0．05），CAF组的表达明显增加（1．26±0．13vs1．04±0．15，P〈0．001），CAF组较PAF组亦明显增加（P〈0．01）。CIC-2的mRNA表达与左房内径、AF持续时间呈正相关[（r=0．441，P〈0．001）（r=0．331，P=0．0C15）]。结论AF患者CIC-1、CIC-2的mRNA表达水平的增加可能是心房肌电重构的分子基础。     

氟伐他汀和缬沙坦联合治疗改善原发性高血压患者高脂餐后纤溶功能

目的观察氟伐他汀和缬沙坦联合治疗对原发性高血压患者高脂餐后血浆纤溶酶原激活物抑制剂1（PAI-1）和组织型纤溶酶原激活剂（t-PA）抗原浓度的即期影响。方法原发性高血压患者53例随机分成对照组（安慰剂n=13）、氟伐他汀组（40mg／d，n=13）、缬沙坦组（80mg／d，n=14）和联合组（氟伐他汀：40mg／d＋缬沙坦：80mg／d，n=13）4组治疗1周，禁食12h后测高脂餐前（空腹，F）、后（4h，P）的血浆可溶性P选择素、PAI-1和t-PA抗原及血脂浓度。4组分别治疗1周后再重复以上实验1次，并测量4组治疗前、后的血压。结果高脂餐后血浆三酰甘油（TG）IF：（1．94±0．91）比P：（3．15±1．48）mmol／L]、可溶性P选择素IF：（259．8±124．0）比P：（345．7±138．4）ng／mL]、PAI-I[F：（36．4±13．1）比P：（48．7±18．5）ng／mL]和t-PA抗原[F：（9．6士3．2）比P：（13．5±6．0）ng／mL]浓度升高，差异有非常显著意义。高脂餐后血浆TG浓度分别与高脂餐后可溶性P选择素（r=0．430）、PAI-1抗原（r=0．421）浓度显著相关（P〈0．01）。治疗1周后，缬沙坦组和氟伐他汀组的高脂餐后血浆可溶性P选择素、PAI-1和t-PA抗原浓度较各自空腹水平差异无统计学意义。联合组的空腹和高脂餐后血浆可溶性P选择素、PAI-1和t-PA抗原浓度较治疗前基础水平显著降低（P〈0．05）。联合治疗一周后也明显地抑制了高脂餐后可溶性P选择素、PAI-1与t-PA，虽然仍有轻度增加，但差异无统计学意义（P〉0．05）。上述指标的变化发生在血脂变化之前。结论与氟伐他汀或缬沙坦的单用相比，极短期两药联合应用有效地降低了原发性高血压患者空腹和高脂餐后的血浆PAI-1和t-PA抗原浓度。     

脂肪分存的顺序及其与胰岛素抵抗的关系

目的探讨高脂饲养SD大鼠脂肪分存的顺序及其与胰岛素抵抗的关系。方法将8周龄雄性SD大鼠随机分为2组：正常饲养组（NC，n=40）、高脂饲养组（HF，n=40）。在不同周龄测定血清、肝脏、肌肉组织中甘油三酯（TG）含量；进行正常血糖高胰岛素钳夹试验评估胰岛素的敏感性；并用定量PCR方法分析肝脏和肌肉中脂代谢调控基因mRNA表达的变化。结果（1）与NC组比较，高脂饲养4周、8周时血TG无明显变化，12周时明显增高[0．52（0．15-1．00）mmol／L vs 0．31（0．09-0．53）mmol／L，P〈0．01]，持续至20周。（2）HF组肝脏TG含量从高脂饲养4周始便明显增高[（34．38±11．12）mg／g vs（1．65±0．37）mg／g，P〈0．01]，一直持续至20周；肌肉TG在高脂饲养4、8、12周均无明显变化，高脂饲养20周时明显增高[（32．24±7．24）mg／g vs （2．77±0．76）mg／g，P〈0．01]。（3）正常血糖高胰岛素钳夹试验表明，HF组高脂饲养4周始葡萄糖输注率（GIR）呈下降趋势，高脂饲养8周时明显下降[（21．81±7．20）mg·kg^-1·min^-1 vs （8．44±1．77）mg·kg^-1·min^-1，P〈0．01]，一直持续至20周。（4）脂代谢调控基因的检测表明，高脂饲养4周时肝脏中合成基因乙酰辅酶A羧化酶（ACC1）的表达无明显增高而氧化基因肉毒碱酰基转移酶（CPT-1）的表达下降20．3％（P〈0．05），肌肉组织ACC2、CPT-1的表达均无明显变化（P〉0．05）；高脂饲养8周时肝脏中ACC1的表达增高20．6％、CPT-1的表达下降27．1％（P〈0．05），肌肉组织ACC2的表达增高18．6％、CPT-1的表达下降19．2％（P〈0．05）；高脂饲养20周时肝脏ACC1表达增高48．3％（P〈0．05）、CPT-1表达无明显变化（P〉0．05），肌肉ACC2表达增高101．1％、CPT-1的表达下降71％（P〈0．05）。结论高脂饲养SD大鼠脂肪分存过程中，肝脏早于肌肉，肝脏TG含量增加可能是胰岛素抵抗的早期标志之一。脂代谢调控基因的表达可能在其中起了重要作用。     

非酒精性脂肪性肝病患者脂联素基因表达的变化

脂肪组织是一个复杂、重要、非常活跃的代谢和内分泌器官。脂肪组织与胰岛素抵抗（insulin resistance，IR）相关的超重和（或）肥胖、2型糖尿病和非酒精性脂肪性肝病（nonalcoholic fatty liver disease，NAFLD）等代谢综合征密切相关，其机制可能是通过脂肪组织储能量和分泌众多的细胞因子和激素起作用。近年研究发现，血清脂联素（adiponectin）水平下降与2型糖尿病和心血管疾病有关，但与NAFLD关系、对脂肪组织脂联素基因表达和NAFLD的关系尚少见报道，本文探讨NAFLD患者的脂肪组织脂联素基因表达变化及血脂联素水平和发病中作用。     

2型糖尿病一级亲属脂联素等与胰岛素抵抗的相关研究

测定糖耐量正常T2DM患者一级亲属35例，及对照组42例的脂联素、抵抗素、TNF-α。结果1．一级亲属组脂联素水平低于正常对照组（12．29±3．64mg／L vs 14．66±3．43mg／L，P〈0．05），而抵抗素、TNF-α水平显著高于正常组（分别是19．02±6．85Pg／ml vs 15．68±6．24pg／ml，P〈0．05；14．12±2．87pg／ml vs 10．43±2．58pg／ml，P〈0．05）；2．一级亲属组IR指数与脂联素呈负相关（r=-0．53，P〈0．05），与抵抗素、TNF-α呈正相关（分别为r=0．62，P〈0．05；r=0．48，P〈0．05）。结论脂联素、抵抗素、TNF-α可能与T2DM患者一级亲属的IR相关。     

Exendin-4改善胰岛素抵抗的作用机制研究

目的探讨exendin-4（exenatide）对高脂诱导胰岛素抵抗（IR）大鼠胰岛素敏感性（IS）改善的机制及对脂肪细胞因子的影响。方法健康雄性SD大鼠随机分为正常饮食组（NC）、高脂组（HF）和高脂＋Exenatide组（HE）。HE组给予exenatide（2μg／kg，Et二次）腹腔注射6周，用静脉胰岛素耐量试验评价各组IS变化，观察各组肌肉和脂肪组织胰岛素信号传导、脂肪细胞因子表达和血浆浓度变化。结果6周后，HE组Lee＇s指数、空腹血浆FFA、TG、TC均较NC组降低（P均〈0．01），IR明显改善；胰岛素刺激后HE组肌肉和脂肪组织IRS-1酪氨酸磷酸化升高（P〈0．05）；HF和HE组血浆内脏脂肪素（visfatin）水平明显降低（P〈0．05，P〈0．01），但HE组脂联素（APN）血浆水平和脂肪组织mRNA表达明显高于HF和NC组（P均〈0．01）。结论Exenatide明显改善了高脂大鼠IR，其胰岛素增敏机制可能与增强IRS-1酪氨酸磷酸化以及对APN、visfatin等脂肪细胞因子的影响有关。     

外周动脉疾病患者脂联素、氧化型低密度脂蛋白与IMT的相关性

目的探讨脂联素在外周动脉疾病患者中与动脉硬化的关系及机制。方法酶联免疫吸附测定（ELISA）法分别测定77例外周动脉疾病患者（包括颈动脉狭窄33例、肾动脉狭窄29例及腹主动脉瘤15例）、33例对照组血浆脂联素及氧化型低密度脂蛋白浓度,超声测定颈动脉内膜中层厚度（intima media thickness,IMT）,分析三个指标之间的相关性。结果平方根转换后外周动脉疾病患者血浆脂联素浓度较对照组显著降低[（2．39±0．07）Sqrtmg／L vs．（3．58±0．14）Sqrt mg／L,P〈0．001],氧化型低密度脂蛋白浓度显著高于对照组[（3．20±0．17）Sqrμxg／Lvs.（1．55±0．24）Sqrtμg／L,P〈0．001）。血浆脂联素与氧化型低密度脂蛋白浓度的平方根呈负相关（r=0．526,P〈0．001）,与颈动脉IMT呈负相关（r=-0．384,P〈0．001）;氧化型低密度脂蛋白浓度的平方根与颈动脉IMT呈正相关（r=0．336,P〈0．001）。偏相关分析校正年龄、吸烟年支数、血糖、血脂指标后,血浆脂联素与氧化型低密度脂蛋白浓度的平方根仍呈负相关（r=-0．235,P〈0．05）,与颈动脉IMT呈负相关（r=0．175,P〈0．05）;血浆氧化型低密度脂蛋白浓度的平方根与颈动脉IMT呈正相关（r=0．157,P〈0．05）。结论血浆脂联素浓度与外周动脉疾病的发生、发展以及机体的氧化应激相关。     

Altered levels of adipocytokines in association with insulin resistance in patients with systemic lupus erythematosus

OBJECTIVE: The metabolic syndrome, closely associated with cardiovascular disease, is characterized by increased insulin resistance (IR). Although accelerated atherosclerosis is frequently observed in systemic lupus erythematosus (SLE), the prevalence and significance of IR remain to be elucidated. We evaluated IR in association with plasma concentrations of adipocytokines in patients with SLE. METHODS: Outpatients with SLE (n = 37) and healthy controls (n = 80) were studied. A value of the homeostasis model assessment index (HOMA-IR) > 2.0 was considered to be IR. Plasma concentrations of adiponectin and tumor necrosis factor-a (TNF-a) were measured by ELISA and leptin by radioimmunoassay. RESULTS: HOMA-IR indices of the SLE patients were significantly higher than those of controls (2.3 +/- 2.3 vs 1.3 +/- 1.0, respectively; p < 0.01), although both groups exhibited a similar body mass index. The prevalence of hypertension and diabetes mellitus was significantly higher in patients with SLE compared with controls (48.6% vs 8.8% and 10.8% vs 0%). Twelve SLE patients (32%) with IR exhibited significantly higher incidence of hypertension and current proteinuria than SLE patients without IR. Plasma leptin, TNF-a, and, unexpectedly, adiponectin levels were higher in SLE patients than controls (adiponectin, 13.7 +/- 5.0 vs 9.5 +/- 3.9 microg/ml). Among the SLE patients, patients with IR showed significantly lower adiponectin levels than patients without IR (10.9 +/- 4.6 vs 15.4 +/- 4.4 microg/ml). Serum levels of adiponectin were significantly correlated inversely with HOMA-IR in SLE patients. CONCLUSIONS: Elevated levels of adiponectin in SLE, despite inverse correlation with IR, suggest the possible involvement of adiponectin in IR and alterations in its effect on insulin sensitivity.     

2型糖尿病患者皮下、大网膜脂肪组织脂联素mRNA表达的定量研究

目的　探讨 2型糖尿病患者皮下及大网膜脂肪组织脂联素 (adiponectin)表达水平及与血脂联素、体重指数、腰臀比 (WHR)、胰岛素敏感性的相关关系。方法　用实时荧光定量RT PCR检测 2型糖尿病患者和非糖尿病患者皮下及大网膜脂肪组织脂联素mRNA的表达水平 ,用ELISA方法测定血浆脂联素水平。结果　 2型糖尿病患者大网膜脂肪组织脂联素mRNA表达水平较非糖尿病组显著下降 (P <0 .0 5 ) ;糖尿病组与非糖尿病组的血浆脂联素水平差异无显著性 ;糖尿病组大网膜脂肪组织脂联素mRNA表达与WHR成负相关 (r=- 0 .5 1,P <0 .0 5 )。糖尿病组血浆脂联素水平与大网膜脂肪组织脂联素mRNA的表达成正相关 (r=0 .5 7,P <0 .0 1)。结论　 2型糖尿病患者大网膜脂肪组织脂联素mRNA表达显著降低。内脏脂肪组织脂联素mRNA的表达水平可以作为胰岛素抵抗的重要参数。     

Increased serum resistin in nonalcoholic fatty liver disease is related to liver disease severity and not to insulin resistance

CONTEXT: The recently discovered hormone resistin is linked to the development of insulin resistance, but direct evidence of resistin levels in humans with nonalcoholic fatty liver disease (NAFLD) is lacking. METHODS: We conducted this study to assess the relationship between serum resistin and NAFLD. We measured serum resistin and biochemical, hormonal, and histological correlates in 28 NAFLD patients, 33 controls, and 30 obese patients [body mass index (BMI), >30 kg/m2] without NAFLD. RESULTS: Resistin and adiponectin expression were measured in sc adipose tissue by quantitative RT-PCR. Resistin was higher in NAFLD patients compared with controls (5.87 +/- 0.49 vs. 4.30 +/- 0.20 ng/ml; P = 0.002) and obese patients (4.37 +/- 0.27 ng/ml; P = 0.002). Increased resistin mRNA was also found in the adipose tissue of NAFLD patients compared with controls and obese subjects. CONCLUSIONS: Both NAFLD and obese patients had lower adiponectin levels, whereas leptin was increased only in the obese group. No correlation was found between resistin and high-sensitivity C-reactive protein, BMI, homeostasis model assessment, insulin, glucose, transaminases, and lipid values. A positive correlation was found between resistin and histological inflammatory score. These data report increased resistin in NAFLD patients that is related to the histological severity of the disease, but do not support a link between resistin and insulin resistance or BMI in these patients.     

Adiponectin mRNA levels in the abdominal adipose depots of nondiabetic women

BACKGROUND: The human adiponectin gene has been implicated in the pathophysiology of obesity, type II diabetes mellitus, dyslipidemia and atherosclerosis. Investigation of the physiological functions of the adiponectin gene in humans was mainly conducted at the levels of plasma proteins or DNA polymorphisms. The depot-specific adiponectin mRNA levels also could be relevant to these physiological functions. OBJECTIVES: The relation between the adipose depot-specific adiponectin mRNA expression levels and various metabolic factors, including BMI, fasting plasma glucose, insulin, triglycerides (TGs) and HDL-cholesterol and insulin resistance index by HOMA, was investigated among 66 nondiabetic women using quantitative real-time PCR. RESULTS: The subcutaneous relative adiponectin mRNA levels (SRAmR) correlated significantly with the omental relative adiponectin mRNA levels (ORAmR) (gamma=0.468, P=0.0001). The SRAmR correlated inversely with the fasting plasma glucose with a borderline significance (gamma=-0.35, P=0.058). On the other hand, the ORAmR correlated negatively with serum TG levels with the adjustment for age (gamma=-0.33, P=0.007) or age plus BMI (gamma=-0.27, P=0.027). CONCLUSION: These results indicate that the adiponectin mRNA levels in different adipose depots were at least related to certain phenotypes of metabolic syndrome. The expression levels of adiponectin in the omental adipose depots are related to TG metabolism.     

Plasma adiponectin is decreased in nonalcoholic fatty liver disease

OBJECTIVES: Nonalcoholic fatty liver disease (NAFLD) is a major cause of liver-related morbidity and is frequently associated with obesity and metabolic syndrome. The recently discovered hormone adiponectin is produced by adipose tissue, and low plasma adiponectin is considered a key factor in the development of the insulin resistance underlying metabolic syndrome. Animal studies suggest that adiponectin may protect against non-alcoholic steatohepatitis, but direct evidence in humans is lacking. We therefore conducted this study to assess the relationship between plasma adiponectin and nonalcoholic fatty liver disease to explore its role in the pathogenesis of this disease. DESIGN AND METHODS: We measured plasma adiponectin and anthropometric, biochemical, hormonal and metabolic correlates in a group of 17 NAFLD patients with diagnosis confirmed by biopsy, and 20 controls with comparable age, body-mass index and sex. Furthermore we compared plasma adiponectin in patients with simple steatosis and steatohepatitis. RESULTS: Plasma adiponectin was significantly lower in NAFLD patients than controls (5.93+/-0.45 vs 15.67+/-1.60ng/ml). Moreover, NAFLD patients were significantly more insulin resistant while having similar serum leptin. Adiponectin was similar in simple steatosis and in steatohepatitis (6.16+/-0.78 vs 5.69+/-0.49ng/ml). An inverse correlation was observed between adiponectin and homeostatic model assessment (HOMA) of insulin resistance (P = 0.008), while adiponectin did not correlate with serum transaminases and lipid values. CONCLUSIONS: These data support a role for low circulating adiponectin in the pathogenesis of NAFLD and confirm the strict association between reduced adiponectin production by adipose tissue, NAFLD and insulin resistance.     

Human adipose tissue cannabinoid receptor 1 gene expression is not related to fat cell function or adiponectin level

CONTEXT: The cannabinoid receptor 1 gene (CNR1) is implicated in adipocyte function. OBJECTIVE: We investigated human adipose tissue CNR1 mRNA in relation to obesity, clinical and metabolic variables, adipocyte function, and adiponectin (ADIPOQ) levels. METHODS: We assessed sc fat biopsies from 96 obese and nonobese subjects and omental fat biopsies from 82 obese and nonobese subjects. RESULTS: The sc and omental adipose CNR1 gene expression were similar in obese and nonobese subjects. No association between either sc or omental adipose CNR1 mRNA levels and body mass index, waist circumference, plasma levels of glucose and insulin, lipids, or blood pressure was found. The sc and omental maximal adrenergic lipolytic activation as well as lipolytic adrenoceptor sensitivity were not related to CNR1 gene expression. Lipogenesis in sc adipocytes also showed no association with CNR1 mRNA levels. Finally, no relation was found between adipose CNR1 gene expression and ADIPOQ mRNA, adipose tissue adiponectin secretion, or circulating adiponectin. CONCLUSION: We found no association of human adipose tissue CNR1 mRNA expression with measures of body fat, metabolic parameters, fat cell function, or ADIPOQ expression. These data do not suggest a major role of human adipose CNR1 in fat cell function or metabolic disease development.     

Associations between plasma adiponectin concentrations and liver histology in patients with nonalcoholic fatty liver disease

OBJECTIVES: To explore associations between plasma adiponectin concentrations and liver histology in patients with nonalcoholic fatty liver disease (NAFLD). DESIGN AND PATIENTS: In a cross-sectional study, we enrolled 60 consecutive NAFLD patients and 60 age-, sex- and body mass index (BMI)-matched healthy controls. MEASUREMENTS: NAFLD (by liver biopsy), plasma adiponectin concentrations, insulin resistance (by homeostasis model assessment, HOMA-IR) and metabolic syndrome (MetS) features. RESULTS: NAFLD patients had a marked decrease in plasma adiponectin concentration (6.1 +/- 2.8 vs. 13.6 +/- 3.8 microg/ml, P < 0.001) compared with matched controls. MetS, as defined by the Adult Treatment Panel III (ATP III) criteria, and its individual components were more frequent among NAFLD patients. The marked differences in adiponectin concentrations that were observed between the groups were little affected by adjustment for age, sex, BMI, HOMA-IR score and MetS components. Notably, decreased adiponectin levels were closely associated with the degree of hepatic steatosis, necroinflammation and fibrosis (P < 0.001 for all) among NAFLD patients. By logistic regression analysis, low adiponectin levels independently predicted hepatic steatosis [odds ratio (OR) 2.3, 95% confidence interval (CI) 1.5-5.8, P < 0.001] and necroinflammation (OR 3.1, 95% CI 1.9-7, P < 0.001), but not fibrosis (P = 0.07), after adjustment for age, sex, BMI, HOMA-IR and MetS components. CONCLUSIONS: NAFLD patients have markedly lower plasma adiponectin concentrations than control subjects. Low adiponectin levels are strongly associated with the severity of liver histology, thus further supporting the hypothesis that adiponectin might be involved in the development of NAFLD.     

维吾尔族肥胖患者脂肪和血清内脂素、脂联素的改变及相关因素

目的 探讨维吾尔族肥胖患者内脂素、脂联素(APN)在腹部网膜、皮下脂肪组织的表达和血清水平改变及其与体重指数(BMI)、腰臀围比(WHR)和血脂的关系.方法 用半定量RT-PCR方法检测41例肥胖患者和20例非肥胖对照脂肪组织内脂素和APN mRNA表达水平,ELISA法检测血清内脂素和APN浓度,并测量腰围(WC)、臀围(HC)、血压(BP)、空腹血糖(FPG)和血脂等.结果 ① 网膜脂肪组织内脂素mRNA表达水平在肥胖组与非肥胖对照组之间差异无显著性,肥胖组APN mRNA表达水平显著低于非肥胖对照组(P<0.05);内脂素、APN在两组网膜和皮下脂肪组织mRNA的表达水平均无显著性部位差异;血清内脂素肥胖组显著高于非肥胖对照组(P<0.05),APN在两组之间比较差异无显著性.② 肥胖组舒张压(DBP)和收缩压(SBP)均显著高于非肥胖对照组(P<0.01和P<0.01),高密度脂蛋白(HDL-C)明显低于非肥胖对照组(P<0.05).③ 网膜脂肪组织内脂素mRNA表达量与血清内脂素、BMI和TG显著正相关,APN mRNA表达量与血清APN显著正相关,与BMI、LDL-C显著负相关.结论 维吾尔族肥胖患者血清内脂素水平升高,网膜和皮下脂肪组织内脂素mRNA表达水平无显著性部位差异;APN mRNA在网膜脂肪组织的表达显著降低,内脂素和脂联素可能在维吾尔人中心性肥胖相关的代谢紊乱性疾病中起一定作用.