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 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.
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.
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.
Diabetic retinopathy (DR) is one of common and specific microvascular complications caused by diabetic mellitus, and remains a serious and common ocular complication leading preventable blindness. At present, the specific pathogenesis of DR is not completely clear, and many factors are involved in its occurrence and development. Adiponectin (APN) is an endogenous cytokine secreted by adipocytes. It is expressed in all layers of retina, especially in the outer layer (rods and cones). It is involved in regulating fatty acid oxidation and glucose metabolism by binding with specific receptors. In recent years, a lot of studies have found that APN can be involved in regulating blood glucose, inhibiting neovascularization, reducing inflammation, dilating blood vessels and improving vascular endothelial function. At present, the specific mechanism of APN in the occurrence and development of DR Remains to be determined. Further research on the level changes and the specific mechanism of action of APN in DR may help to identify the characteristic metabolic changes of DR, thus providing new biomarkers for the diagnosis of DR, while helping to promote the innovation of the treatment of DR.
The exact pathophysiological mechanisms of diabetic retinopathy (DR) remain elusive. The inflammatory reaction, retinal vascular leakage and retinal neovascularization are main features of DR. Adiponectin (APN) is an endogenous biological active protein secreted by adipocytes. It can increase insulin sensitivity, regulate blood glucose and lipid metabolism, and has anti-inflammation and anti-neovascularization functions. It may be involved in the development of DR. This review summarized the studies on the association between APN and DR in recent years.
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.
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。