Objective To investigate the role of inflammatory factors like serumleptin, adiponectin,interleukin-6( IL-6) , and C-reactive protein ( CRP) in the systemic inflammatory response of smokinginduced COPD. Methods Thirty male Wistar rats were randomly divided into three groups, ie. a high-dose smoking group, a low-dose smoking group, and a control group. Serum leptin, adiponectin, IL-6, and CRP levels were measured by ABC-ELISA. Results The serum leptin and adiponectin levels in both smoking groups decreased significantly compared with the control group( P lt; 0. 05) , while the difference was not significant between the two smoking groups ( P gt; 0. 05) . The serum IL-6 and CRP levels in both smoking groups increased significantly compared with the control group( P lt; 0. 05) , which were higher in the highdosesmoking group than those in the low-dose smoking group( P lt;0. 05) . Conclusions Smoking increases the serum levels of IL-6 and CRP, but reduces the serum levels of leptin and adiponectin in rats. These results suggest that leptin, adiponectin, IL-6, and CRP may be involved in the systemic inflammatory response of smoking-induced COPD.
Objective To investigate the effect of adiponectin on proliferation of airway smooth muscle cells( ASMCs) , and explore its possible mechanism. Methods ASMCs were derived fromrat airway tissue and were cultured in vitro. RT-PCR was used to verify the expression of adiponectin receptors on ASMCs. Then ASMCs were treated with adiponectin at different concentrations( 5, 10, 20, 40, 80 μg/mL) for different periods of time( 1, 12, 24, 48, 72 hours) , respectively. The absorbsence ratios of adiponectin at different concentrations were determined by MTT assay. The adenosine monophosphate-activated protein kinase( AMPK) and phosphorylated AMPK( pho-AMPK) in ASMCs were quantified by Western blot after being treated with adiponectin at different concentrations ( 5, 10, 20, 40 μg/mL) for 48 hours. ResultsThe inhibition of adiponectin on ASMCs was showed in dose-dependent manner( r = 0. 324, P lt; 0. 01) and time-dependent manner( r = 0. 607, P lt; 0. 05) . Western blot indicated that the expression of pho-AMPK increased with the increased concentrations of adiponectin( r =0. 607, P lt; 0. 01) . The ratio of pho-AMPK/AMPK were ( 27. 66 ±1. 03) % , ( 31. 91 ±0. 86 ) %, ( 75. 52 ±2. 67) % , and ( 84. 50 ±1. 05) % ,respectively, with significant differences between each concentrations of adiponectin( P lt; 0. 05) . There was no expression of pho-AMPK in the control group. Conclusion Adiponectin can significantly inhibit ASMCs’proliferation by activating AMPK.
【Abstract】 Objective To observe the plasma levels of adiponectin and interleukin-17 ( IL-17) in patients with chronic obstructive pulmonary disease ( COPD) at acute exacerbation or stable stage, and analyze their relationship. Methods Sixty male COPD patients with normal weight ( with BMI range of 18. 5-24. 9 kg/m2 ) were enrolled, including 30 patients with acute exacerbations of COPD ( AECOPD) and 30 patients with stable COPD. Twenty healthy nonsmoking male volunteers were included as controls. The plasma levels of adiponectin and IL-17 as well as lung function ( FEV1% pred and RV% pred) were measured in all subjects. Results The concentrations of adiponectin and IL-17 were significantly higher in the AECOPD patients than those of the patients with stable COPD and the contro1s ( P lt; 0. 001) . Theconcentrations of adiponectin and IL-17 were significantly higher in the patients with stable COPD than those of the controls ( P lt;0. 01) . Adiponectin was positively correlated with IL-17 in the AECOPD patients ( r =0. 822, P lt;0. 001) and in the patients with stable COPD ( r =0. 732, P lt;0. 001) . Adiponectin was positivelycorrelated with RV% pred in the AECOPD patients ( rs = 0. 764, P lt;0. 001) and in the patients with stable COPD ( rs =0. 967, P lt;0. 001) . There was no significant relationship between adiponectin and FEV1% pred ( P gt;0. 05) . Conclusions The plasma level of adiponectin in COPD patients is elevated which is relatedwith excessive inflation of lung. Adiponectin may be involved in the process of inflammation in COPD as a new pro-inflammatory cytokine.
Objective To comprehend the pathological features and possible pathogenesis of avascular necrosis of the femoral head (ANFH) by morphology and immunohistochemical observation of osterix (OSX) and adiponectin through in vitro traumatic and non-traumatic ANFH specimens, so as to provide a theoretical basis for cl inical treatment. Methods Sixty-six ANFH specimens were collected from 66 cl inical cases undergoing hip replacement surgery. Twenty-four cases of traumatic ANFH (group A) included 17 males and 7 females, aged 21 to 70 years with an average of 56.5 years; 23 cases of steroid-induced ANFH (group B) included 16 males and 7 females, aged 56 to 72 years with an average of 61 years; and 19 cases of alcohol ic ANFH (group C) were males, aged 55 to 67 years with an average of 58.5 years. Bone tissue was got from weight-bearing and non-weight-bearing area of the femoral head respectively. The basic pathological changes was observed by HE staining under the optical microscope, and the percentage of empty bone lacuna and the percentage of trabecular bone area were calculated. The morphological changes of ANFH in different groups were observedby scanning electron microscope (SEM). OSX and adiponectin expression were detected by immunohistochemical technique. Results Gross of the femoral head surface in each group was rough, collapse, articular cartilage loss, osteophyte formation; cross section: dark red in group A, and yellow in groups B and C. HE staining showed that weight-bearing area of ANFH have similar morphological features in three groups. In non-weight-bearing area of groups B and C, the fat cells in bone marrow markedly increased and were hypertrophic; however there were more fibrous tissue in group A. There were statistically significant differences (P lt; 0.001) in the percentage of empty bone lacuna of the weight-bearing and non-weight-bearing area among three groups. There were no statistically significant differences (P gt; 0.05) in the percentage of trabecular bone area among three groups. The SEM observation showed that three groups had similar pathological changes. Brown granules for OSX and adiponectin positive substance were mainly located in the osteoblast of bone marrow of the femoral head. There was statistically significant difference (P lt; 0.05) in the average absorbency (A) value of OSX between group A and groups B, C, but there was no statistically significant difference (P gt; 0.05) between groups B and C. While there was no statistically significant difference (P gt; 0.05) in the A value of adiponectin among three groups. Conclusion Hormones and alcohol necrosis have more obviously fatty degeneration, but the repair capacity of traumatic femoral head necrosis is ber than that of hormones and alcohol necrosis. Alcohol and hormones have inhibitory action on the OSX-mediated osteogenic differentiation. Hormones and alcohol may not affect osteoblast expressing adiponectin and its receptors.
Objective To evaluate the relationship between the single nucleotide polymorphisms (SNPs) of the adiponectin gene +45 in exon 2 and type 2 diabetes mellitus (T2DM) in Chinese population via meta-analysis. Methods Databases including PubMed, Ovid, CBM, VIP, CNKI, and WanFang Data were searched from inception to June 2012, and the references of articles were also retrieved to collect case-control studies about the correlation of SNPs of the adiponectin gene +45 in exon 2 and T2DM in Chinese population. According to the self-designed inclusion and exclusion criteria, two reviewers screened articles, extracted data, and assessed the quality of the included studies independently. Then meta-analysis was performed STATA 11.0, with stability evaluated by both stratified analysis and sensitivity analysis. Moreover, Begg’s funnel plot and Egger’s method were used to assess the published bias of articles. Results 21 articles involving 22 studies were included (3272 T2DM cases and 2597 controls). There were significant differences between the two groups in dominant, recessive and addictive genetic models, and the pooled ORs (95% CI) were 1.36 (1.04, 1.78), 2.07 (1.55, 2.75), and 2.44 (1.59, 3.75), respectively. Conclusion The genetic single nucleotide polymorphisms of the adiponectin +45 in exon 2 is associated with type 2 diabetes in Chinese population. G allele of APM1 is a risk factor for type 2 diabetes, no matter in dominant, recessive or addictive genetic models.
【摘要】 目的 探讨胰岛素强化治疗对2型糖尿病（type 2 diabetes mellitus，T2DM）患者血清脂联素（adiponectin，APN）的影响。 方法 2007年7—12月，研究纳入连续使用胰岛素治疗至少3个月但血糖控制欠佳[6.5%≤糖化血红蛋白（hemoglobin A1c， HbA1c）≤11.0%]的T2DM患者40例，其中男18例，女22例；年龄29~〖JP2〗69岁；平均诊断T2DM病史11年。治疗方案为进行16周的胰岛素强化治疗，血糖控制目标为空腹血糖≤7 mmol/L，〖JP〗餐后2 h血糖≤8 mmol/L。分别于强化治疗前、强化治疗4周后及强化治疗16周后测定HbA1c以及血清APN水平。 结果 与强化治疗前相比，胰岛素治疗4周后空腹及三餐后2 h血糖明显下降（Plt;0.05），但HbA1c和血清APN水平差异无统计学意义（Pgt;0.05）；强化16周后，HbA1c水平明显低于治疗前和治疗4周后且差异具有统计学意义（Plt;0.05），APN水平高于治疗前和治疗4周后且差异有统计学意义（Plt;0.05）。体质量指数在强化治疗16周后明显增加且与强化治疗前和强化治疗后4周相比差异具有统计学意义（Plt;0.05）。APN与空腹血糖（b=-0.225，P=0.013）、早餐后2 h血糖（b=-0.229，P=0.012）呈负相关。 结论 胰岛素强化治疗可以提高T2DM患者血清APN水平。【Abstract】 Objective To investigate the effect of intensive insulin therapy on serum adiponectin (APN) level in patients with type 2 diabetes mellitus (T2DM). Methods Forty patients with T2DM who had undergone insulin therapy for at least three months but with their blood glucose poorly controlled [glycosylated hemoglobin Alc (HbA1c) level ranged from 6.5% to 10.0%] from July to December 2007 were enrolled in this study. There were 18 males and 22 females with their age ranged from 29 to 69 years. They had an average time of T2DM history of 11 years. Intensive insulin therapy was carried out for 16 weeks with a target of less than 7 mmol/L for fasting blood glucose and 8 mmol/L for postprandial blood glucose. HbA1c and serum adiponectin concentrations were detected at baseline, at week 4 after intensive therapy and at the end of the study. Results After 4 weeks of intensive blood glucose control, fasting and postprandial blood glucose levels decreased significantly (Plt;0.05), but the HbA1c and serum APN concentrations did not reduce remarkably (Pgt;0.05). After 16 weeks of treatment, the level of HbA1c was significantly lower than those at baseline and 4 weeks after treatment (Plt;0.05), and serum APN concentration increased significantly (Plt;0.05), compared with those two time points. However, an evident increase of body mass index (BMI) was found while compared with BMI at baseline and 4 weeks after treatment (Plt;0.05). The linear regression analysis indicated that APN was negatively associated with fasting blood glucose (b=-0.225,P=0.013) and blood glucose level 2 hours after breakfast (b=-0.229,P=0.012). Conclusion Intensive insulin therapy can improve serum adiponectin level in type-2 diabetic patients.
目的:观察缬沙坦治疗前、后高血压合并糖尿病患者血清脂联素的变化。方法:将我院高血压合并糖尿病患者60例随机分为两组,然后分别给予缬沙坦或氨氯地平治疗至少8周,分析治疗前、后两组间的血清脂联素变化。结果:与治疗前相比较,缬沙坦组显著降低了血清脂联素(Plt;0.01),而氨氯地平组治疗前、后的脂联素改变无显著差异性。结论:与氨氯地平比较,缬沙坦在降压的同时,显著降低了血清脂联素水平。
目的:探讨盐敏感性高血压患者胰岛素抵抗与脂联素代谢异常的关系。方法:对100例高血压患者采用急性盐水负荷试验,确定65例为盐敏感性(SS)高血压患者,35例为盐不敏感性(NSS)高血压患者,选定正常人50例为对照组,分别测其胰岛素水平、血脂、血尿酸及脂联素水平。结果:高血压患者存尿酸、胆固醇、甘油三酯水平升高(Plt;0.01),SS组较NSS组的血尿酸、血胆固醇、血甘油三脂增高(Plt;0.01)。SS组脂联素［(6.04±2.08)ng/mL］,较NSS组［(7.89±3.35)ng/mL(Plt;0.01)］降低,且SS组存在胰岛素抵抗,HOMA指数分别为［2.54±0.53,2.21±0.55(Plt;0.01)］。血浆脂联素水平与胰岛素抵抗指标存在正相关,r=-0.36,(Plt;0.01)。结论:盐敏感性高血压患者存在胰岛素抵抗及脂联素降低,胰岛素抵抗可能是其他代谢异常及脂联素降低的基础。
摘要:目的: 观察格列美脲对2型糖尿病患者心血管的保护作用并探讨其可能的机制。 方法 :112例T2DM患者随机分为格列美脲组(格列美脲+二甲双胍)和对照组(格列本脲+二甲双胍),观察治疗前后两者空腹及餐后两小时血糖(FBG,2hPBG)、糖化血红蛋白(HbA1c)、空腹胰岛素(FINS)、HOMA模型胰岛素抵抗指数(HOMAIR)、甘油三脂(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDLC)、低密度脂蛋白胆固醇(LDLC)、同型半胱氨酸(HCY)、血浆脂联素的变化。 结果 :两组患者的TC、LDLC、TG、FBG、2hPBG都较治疗前降低,连续服用6个月以上格列美脲的T2DM患者其血浆HCY、HOMAIR、血糖水平明显下降,血浆脂联素水平明显升高,与对照组相比差异有统计学意义(〖WTBX〗P lt;005)。 结论 :格列美脲能降低多项心血管危险因子水平,对血脂、HCY和动脉粥样硬化都有良性调节作用,其作用基础可能与改善胰岛素抵抗,增加血浆脂联素相关。Abstract: Objective: To observe the protective effects and to explore mechanisms of glimepiride on cardiovascular system of Type 2 Diabetes Mellitus. Methods : 112 patients with type 2 diabetes mellitus were randomly divided into treatment group (glimepiride combined with metformin) and control group (glibenclamide combined with metformin). The fasting blood glucose (FBG), 2hPBG, hemoglobin A1c (HbA1c), FINS, HOMAIR, blood lipid (TC, TG, LDLC and HDLC), HCY (homocysteine) and adiponectin were detected before and after treatment. Results : In all cases, the level of TC、LDLC、TG、FBG、2hPBG were decreased after treated with glimepiride or glibenclamide combined with metformin for 6 monthes. Moreover, the level of HCY, HOMAIR and blood glucose were decreased and the level of adiponectin was increased significantly than that of in control group (Plt;005). Conclusion : Glimepiride showed the effective on decreasing the risk factor of cardiovascular system disease with regulation of blood lipid, HCY, and improve the atherosclerosis. The effective of glimepiride on cardiovascular system was relation to improved the insulin resistance and increase the adiponectin.