Myocardial remodeling is a common pathological physiology change for a variety of heart diseases under stimulation such as stress or ischemia. The engine body will release a lot of cytokines to promote the change of myocardial structure and ultimately lead to heart failure. Myocardial remodeling includes myocardial cells remodeling and the extracellular matrix remodeling. In recent years, we find that the function of adipose tissue is not only about energy storage, buffering to protect, supporting and filling, but also has a powerful function of secretion. Adipose tissue can secrete various adipocytokines, such as leptin, adiponectin, visfatin, omentin, angiotensin Ⅱ, and so on. Current studies have shown that adipocytokines and myocardial remodeling are intimated. And this article will summarize the function of adipocytokines on myocardial remodeling.
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。
Objective To explore the correlation of adiponectin rs2241766 gene polymorphism and colorectal cancer. Methods Case-control studies about correlation of adiponectin rs2241766 gene polymorphisms and colorectal cancer were searched by computer retrieval on PubMed, Sciencedirect, Embase, the Cochrane Database, OVID Medline, Springer Link, EBSCO Database, CNKI, VIP, Wanfang, and Chinese Biomedicine Database, the retrieval time was from inception of database to September 30, 2017. At the same time, collected similar literatures and references by manual retrieval. Two independent researchers took the mask of study selection and data extraction, Review Manager 5.3 software was used on calculation results with the OR value and 95% confidence interval (95% CI), on the condition of 5 kinds of gene models. Results A total of 10 case-control studies were included, including 3 460 cases of colorectal cancer and4 170 controls. Results of meta-analysis showed the effect of 5 kinds of model. ① Allele gene model (G vs T): in general population and Yellow race, allele gene model was related to occurrence of colorectal cancer [ORtotal=1.15, 95% CI was (1.07, 1.24), P=0.000 1; ORYellow race=1.16, 95% CI was (1.08, 1.26), P=0.000 1], but there was no significant difference on relationship between allele gene model and occurrence of colorectal cancer for White [ORWhite=1.08, 95% CI was (0.89, 1.30), P=0.44]. ② Dominant gene model (TG+GG vs TT): in general population and Yellow race, dominant gene model was related to occurrence of colorectal cancer [ORtotal=1.23, 95% CI was (1.12, 1.35), P<0.000 1;ORYellow race=1.24, 95% CI was (1.12, 1.37), P=<0.000 1], but there was no significant difference on relationship between dominant gene model and occurrence of colorectal cancer for White [ORWhite=1.17, 95% CI was (0.93, 1.46), P=0.17]. ③ Implicit gene model (GG vs TT+TG): there was no significant difference on relationship between implicit gene model in 3 kinds of population and occurrence of colorectal cancer [general population: ORtotal=1.09, 95% CI was (0.92, 1.30), P=0.32; White: ORWhite=0.77, 95% CI was (0.46, 1.28), P=0.31; Yellow race: ORYellow race=1.15, 95% CI was (0.95, 1.39), P=0.15]. ④ Codominant gene model (TG vs TT): in general population and Yellow race, codominant gene model was related to occurrence of colorectal cancer [ORtotal=1.20, 95% CI was (1.10, 1.32), P<0.000 1;ORYellow race=1.19, 95% CI was (1.08, 1.32), P=0.000 6], but there was no significant difference on relationship between codominant gene model and occurrence of colorectal cancer for White [ORWhite=1.25, 95% CI was (0.99, 1.58), P=0.06]. ⑤ Superdominant gene model (TT+GG vs TG): in general population and Yellow race, superdominant gene model was related to occurrence of colorectal cancer [ORtotal=0.83, 95% CI was (0.76, 0.91), P<0.000 1;ORYellow race=0.84, 95% CI was (0.76, 0.93), P=0.000 6], but there was no significant difference on relationship between superdominant gene gene model and occurrence of colorectal cancer for White [ORWhite=0.80, 95% CI was (0.63, 1.01), P=0.06]. Conclusion The polymorphism of adiponectin gene rs2241766 is related to the occurrence of colorectal cancer in the Yellow race, but there is no significant correlation in White.
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。
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.
【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 measure the serum level of adiponectin and explore its clinical implication in patients with asthma in acute exacerbation and remission phase. Methods 97 patients with asthma were recruited, including 50 patients with asthma in acute exacerbation and 47 patients in remission phase fromOctober 2010 to September 2011. 27 healthy nonsmoking volunteers of normal weight ( BMI range of 18.5-24. 9 kg/m2 ) were included as control. The concentrations of adiponectin and tumor necrosis factor alpha ( TNF-α) in serum were measured by enzyme-linked immunosorbent assay ( ELISA) . The lung function was tested in all subjects. The correlations between adiponectin, TNF-αand lung function were investigated. The data was analyzed using SPSS 19. 0 software. Variables were compared with one-way ANOVA. The correlations between variables were analyzed using Peason’s correlation coefficient or Spearman correlation coefficient.Results Serum adiponectin level was significantly lower in the patients with asthma in acute exacerbation [ ( 246 ±1. 21) ng/mL] than that in the healthy subjects [ ( 9. 64 ±4. 88)ng/mL] and the patients in remission phase [ ( 3. 79 ±0. 96) ng/mL] ( P lt; 0. 01) , while serum adiponectin level was also significantly lower in the patients in asthma remission phase than that in the healthy subjects ( P lt; 0. 01) . The serum adiponectin level in the patients with asthma in acute exacerbation or in asthma remission phase was negatively correlated with the serum TNF-α level ( P lt; 0. 01) , and was positively correlated with FEV1 /predicted value ( P lt; 0. 01) . Conclusions The serum adiponectin is reduced in asthma patients and may play a protective role in asthma.