非肥胖2型糖尿病患者血清内脂素与不同阶段糖尿病肾病的关联性研究

目的研究非肥胖2型糖尿病患者血清内脂素(visfatin)与尿微量白蛋白/肌酐(ACR)之间的相关性,探讨内脂素在不同阶段糖尿病肾病中的改变。方法收集体重指数(BMI)28 kg/m2的2型糖尿病患者90例,按照尿ACR分为单纯糖尿病组30例(T2DM组,尿ACR30μg/mg),微量蛋白尿组30例(DN1组,尿ACR30~300μg/mg),大量蛋白尿组30例(DN2组,尿ACR300μg/mg),健康体检人员组(对照组)30例,测定血清内脂素及血脂、血糖等生化指标。结果非肥胖2型糖尿病患者组血清内脂素水平显著高于对照组(P0.01),糖尿病肾病患者组血清内脂素水平显著高于单纯糖尿病组(P0.01),其中大量蛋白尿组血清内脂素水平显著高于微量蛋白尿组(P0.01)。血清内脂素与尿ACR水平呈正相关(r=0.558,P0.01)。结论非肥胖的2型糖尿病患者血清内脂素水平升高,与尿ACR密切相关,随着糖尿病肾病加重,内脂素也逐渐升高。内脂素有希望作为糖尿病肾病的治疗靶点。     

2型糖尿病患者血清脂联素和内脂素水平与糖尿病肾病的相关性

目的评估2型糖尿病患者血清脂联素和血清内脂素水平与糖尿病肾病间的相关性。方法 2型糖尿病患者96例,根据尿蛋白及尿微量白蛋白的水平分为单纯糖尿病组(36例)和糖尿病肾病组(60例)。同时,以同期行常规体检的健康者30例为对照组。分析和比较各组受试者的血清脂联素和内脂素水平,筛选可用于预测2型糖尿病肾病发生的血清标记物。结果糖尿病患者的血清脂联素均明显低于对照组,血清内脂素水平均明显高于对照组(P<0.05)。而且,糖尿病肾病组血清脂联素和内脂素水平均明显高于单纯糖尿病组(P<0.05)。进一步多因素Logistic回归分析显示,血清内脂素是2型糖尿病患者发生糖尿病肾病的独立危险因素。结论血清脂联素水平降低和血清内脂素水平升高与2型糖尿病肾病的发生密切相关,血清内脂素水平升高可能预示2型糖尿病患者糖尿病肾病的发生或加重。     

2型糖尿病患者一级亲属血清脂联素水平及相关因素研究

糖尿病存在明显的家族遗传易感性。糖尿病一级亲属（FDR）的患病率较一般人群高5～21倍。胰岛素抵抗是2型糖尿病的重要致病因素，有遗传易感性的个体（如有2型糖尿病家族史者）早期即可能存在胰岛素抵抗。脂联素与动脉粥样硬化、胰岛素抵抗、肥胖等疾病存在重要相关性。本研究选取2型糖尿病患者的一级亲属为研究对象，探讨脂联素水平及其影响血浆脂联素水平的相关因素。     

2型糖尿病的非糖尿病一级亲属的血管内皮功能受损

2型糖尿病患者及非糖尿病的2型糖尿病一级亲属血浆一氧化氮和内皮素1水平下降,且与肥胖、胰岛素抵抗呈正相关。     

血浆内脂素在冠心病合并2型糖尿病患者中的表达

目的探讨血浆内脂素在冠心病合并2型糖尿病患者中的表达。方法 90例经过冠状动脉造影确诊为冠心病患者(冠心病组)中,其中合并2型糖尿病患者(冠心病合并2型糖尿病组)51例,不合并2型糖尿病患者(冠心病不合并2型糖尿病组)39例;另外选择32名健康者作为对照组。检测所有入选人群的血浆内脂素的水平。结果不合并2型糖尿病组的内脂素水平明显高于对照组(P<0.01)。冠心病组各亚组间比较,合并2型糖尿病组的内脂素高于不合并2型糖尿病组(P<0.01),血浆内脂素水平随着冠状动脉病变支数的增加而升高,各亚组间的比较差异有统计学意义(P<0.01)。冠心病组血浆内脂素水平与冠状动脉病变支数呈正相关(P<0.01)。结论冠心病患者血浆内脂素水平明显高于健康者,合并2型糖尿病者血浆内脂素水平升高更明显,而且与冠状动脉病变程度密切相关。     

糖尿病患者非糖尿病子女糖尿病相关危险因素调查

目的分析糖尿病患者中非糖尿病子女糖尿病的相关危险因素。方法选择2013—2014年该地区常住人口中2型糖尿病患者一级亲属1 000名作为研究对象,对所有患者进行资料分析,并采用Logistic回归方程计算,分析糖尿病患者非糖尿病子女糖尿病的相关危险因素。结果 2013—2014年该地区常住人口中2型糖尿病患者一级亲属共1 000名,其中患糖尿病者387例,占38.70%。造成糖尿病患者一级亲属患糖尿病的危险因素在肥胖、冠心病、高血脂以及高血压中差异有统计学意义(P0.05)。将上述有差异资料带入Logistic回归方程计算,发现均属于糖尿病患者一级亲属患糖尿病的危险因素。结论糖尿病患者一级亲属患糖尿病的概率较高,导致其患糖尿病危险因素很多,可根据患者具体情况进行干预,做好相关防护措施。     

内脂素与糖尿病大血管并发症的关系

内脂素是一种主要由内脏脂肪细胞分泌的蛋白质细胞因子,具有调节糖脂代谢、炎症等多种生物学活性.临床研究发现肥胖、2型糖尿病和代谢综合征患者血清中内脂素显著增高,其中伴动脉粥样硬化患者更为显著,从而推测血清中内脂素可能与糖尿痛大血管并发症的发生密切相关.文章拟时内脂素的生物学效应及在糖尿病大血管并发症发生发展中的作用进行综述.     

2型糖尿病一级亲属脂联素和胰岛素抵抗与冠心病相关性研究

目的 探讨2型糖尿病患者一级亲属正常糖耐量个体中脂联素水平的变化,研究脂联素和胰岛素抵抗与冠心病的关系.方法 对2型糖尿病患者一级亲属正常糖耐量合并冠心病患者、无冠心病患者、正常人进行血压、空腹血糖(FPG)、胰岛素(FINS)、甘油三酯(TG)、瘦素(Leptin)及脂联素的测定.结果 2型糖尿病一级亲属合并冠心病组和无冠心病组血清脂联素水平低于正常对照组,合并冠心病组血清脂联素水平低于无冠心病组.血清脂联素与血压、TG、Leptin、胰岛素抵抗指数呈负相关.结论 血清脂联素可能在2型糖尿病一级亲属胰岛素抵抗及心血管并发症的发生发展中有重要作用.     

2型糖尿病家系非糖尿病一级亲属脂联素水平与胰岛素抵抗和动脉粥样硬化相关性研究

检测了 2型糖尿病非糖尿病一级亲属组和正常对照组脂联素水平、内皮依赖性舒张功能和颈总动脉内膜中层厚度。结果显示 2型糖尿病家系非糖尿病一级亲属肥胖者脂联素水平降低 ,并且低脂联素与胰岛素抵抗密切相关     

不同糖耐量人群及糖尿病患者血浆内脂素与血糖及胰岛功能的关系研究

目的探讨不同糖耐量人群血浆内脂素的变化及其与体重指数(BMI)、腰围、血糖、胰岛素抵抗指数、胰岛B细胞功能、血脂等的关系。方法2006年4月至2006年10月在南京医科大学第一附属医院门诊常规健康体检及糖尿病初次就诊者95名,按WHO1999糖尿病诊断标准分为初诊2型糖尿病组(53例)、糖耐量减退组(7例)、正常糖耐量组(35名);以WHO1998肥胖诊断标准分为超重或肥胖组(50名)、正常体重组(45名)。检测受试者BMI、腰围、血压,测定空腹血浆内脂素、血糖、血脂、胰岛素等。结果初诊2型糖尿病患者空腹血浆内脂素明显高于正常糖耐量组(P<0.01)。超重或肥胖组与正常体重组间血浆内脂素差异无显著性意义。人群中血浆内脂素与空腹血糖(r=0.338,P<0.01)、餐后2h血糖(r=0.340,P<0.01)、胰岛素抵抗指数(r=0.227,P<0.05)呈正相关,与胰岛素分泌指数(HOMA-B)呈负相关(r=-0.296,P<0.05)。在2型糖尿病组,血浆内脂素与糖化血红蛋白(HbA1c)呈正相关(r=0.356,P<0.01)。多元线性逐步回归分析表明,餐后2h血糖是影响血浆内脂素的独立相关因素。结论初诊2型糖尿病患者血浆内脂素显著升高,可能是机体针对体内血糖增高、胰岛功能受损所发生的一种代偿效应。     

糖尿病和肥胖症患者网膜脂肪组织中的内脂素表达及其影响因素

目的探讨糖尿病、肥胖症患者网膜脂肪组织细胞内脂素的表达及其影响因素。方法选择糖尿病组、肥胖症组、健康对照组各60例,测定血清内脂素、脂联素、肿瘤坏死因子α（TNF-α）浓度。同时,选取三组共66例（糖尿病组23例、肥胖症组22例、对照组21例）行外科手术时切割的各内脏器官网膜脂肪组织提取总mRNA,然后进行Northern b lot印迹技术研究,分析内脂素mRNA差异表达以及与其他脂肪因子的相关关系。结果糖尿病和肥胖症患者血清内脂素浓度较对照组明显升高（P均〈0.01）,糖尿病、肥胖症血清内脂素浓度与TNF-α呈正相关（r=0.441,P=0.045;r=0.541,P=0.037）。网膜脂肪组织中内脂素mRNA的灰度值与血清内脂素、TNF-α水平呈正相关（r=0.771,P=0.021;r=0.500,P=0.041）。结论内脂素在2型糖尿病内脏脂肪及血清中高表达,TNF-α可能促进内脂素表达。     

Reduced plasma visfatin/pre-B cell colony-enhancing factor in obesity is not related to insulin resistance in humans

CONTEXT: Visfatin was recently identified as a protein highly expressed and secreted in adipose tissue with insulin-mimetic effect and is a candidate hormone to help explain the association among adipose tissue expansion, insulin resistance, and type 2 diabetes. OBJECTIVE: The objective of the study was to assess expression of visfatin in lean and obese subjects and in sc and visceral adipose tissue and moreover to explore the role of visfatin on insulin resistance in humans. DESIGN: We measured circulating visfatin and its mRNA expression in sc adipose tissue (SAT) in lean and obese subjects. Furthermore, we measured visfatin mRNA in visceral adipose (VAT) and SAT by quantitative RT-PCR. Finally, plasma visfatin and its mRNA in SAT were measured under free fatty acid-induced insulin resistance in healthy subjects. RESULTS: Plasma visfatin and its mRNA in SAT were significantly lower in obese subjects, compared with normal-weight controls. Both circulating visfatin and SAT visfatin mRNA were negatively correlated with body mass index, whereas no correlation was found with homeostasis model assessment. Significantly higher visfatin mRNA was found in VAT of obese subjects, compared with lean controls. Interestingly, visfatin mRNA in VAT was positively correlated with BMI. Elevation of free fatty acid induced a condition of insulin resistance but did not affect either circulating visfatin or its mRNA. CONCLUSIONS: Our findings show that, in human obesity, plasma visfatin is reduced, whereas visfatin mRNA is differentially regulated in SAT and VAT. Visfatin is not related to insulin resistance either as assessed by homeostasis model assessment or during lipid infusion.     

Increased plasma visfatin concentrations in morbidly obese subjects are reduced after gastric banding

CONTEXT: The insulin-mimetic adipocytokine visfatin has been linked to obesity. The influence of weight loss on plasma visfatin concentrations in obese subjects is unknown yet. OBJECTIVES: In this study we investigated whether plasma visfatin concentrations are altered by weight loss in patients with obesity. DESIGN AND PATIENTS: In a prospective study, fasting plasma visfatin, leptin, and adiponectin concentrations were measured before and 6 months after gastric banding in 31 morbidly obese patients aged 40 +/- 11 yr with a body mass index (BMI) of 46 +/- 5 kg/m(2). Fourteen healthy subjects aged 29 +/- 5 yr with a BMI less than 25 kg/m(2) served as controls. RESULTS: Visfatin plasma concentrations were markedly elevated in obese subjects (0.037 +/- 0.008 microg/ml), compared with controls (0.001 +/- 0.000 microg/ml, P < 0.001). Gastric banding reduced BMI to 40 +/- 5 kg/m(2), visfatin to 19.2 +/- 10.9 ng/ml, and leptin from 39.0 +/- 12.4 to 29.7 +/- 10.0 ng/ml and increased adiponectin from 0.015 +/- 0.007 to 0.017 +/- 0.007 microg/ml (all P < 0.05) after 6 months. Insulin sensitivity as estimated by the homeostasis model assessment insulin resistance index was unchanged from 5.8 +/- 3.1 to 4.6 +/- 1.9 (P = 0.13), but individual changes of insulin resistance and visfatin were significantly associated (P < 0.05, r = -0.43). CONCLUSIONS: Elevated plasma visfatin concentrations in morbidly obese subjects are reduced after weight loss. This may be related to changes in insulin resistance over time.     

吡格列酮与二甲双胍对初诊肥胖2型糖尿病患者血清内脏脂肪素影响的研究

目的观察吡格列酮与二甲双胍对初诊肥胖T2DM患者血清内脏脂肪素（visfatin）水平的影响,探讨visfatin与T2DM发病的关系和药物的治疗机制。方法100例初诊肥胖T2DM患者随机分为吡格列酮组50例,每日口服盐酸吡格列酮片30mg,二甲双胍组50例,每日早晚口服二甲双胍缓释片500mg,疗程24周。结果吡格列酮组空腹血清visfatin、IR、TG较用药前明显降低,B细胞功能有改善（P〈0．05或P〈0．01）。二甲双胍组血清visfatin、TG无统计学改变。两组治疗后比较,吡格列酮组的visfatin、IR、TG降低明显,差异有统计学意义（P〈0．05或〈0．01）,但二甲双胍组的BMI较吡格列酮组下降更明显（P〈0．05）。结论对初诊肥胖T2DM患者吡格列酮与二甲双胍均能较好地控制血糖,吡格列酮还能明显降低血清visfatin的水平,提示吡格列酮通过下调visfatin水平发挥抗炎作用。     

不同血糖状态人群血浆内脂素水平及其相关因素

空腹血浆内脂素水平在正常糖耐量、糖耐量受损或空腹血糖受损、2型糖尿病组分别为[(17.64±1.37,27.423±1.34和26.55±1.64)μg/L,P<0.05],但与肥胖无关.血浆内脂素水平与HbA1c呈正相关(r=0.317,P<0.01).多元线性逐步回归分析表明HbA1c、空腹血糖是影响血浆内脂素的独立相关因素.提示血浆内脂素水平与糖代谢状态有关,可能在2型糖尿病的发生、发展中具有一定的作用.     

The visfatin gene is associated with glucose and lipid metabolism in a Chinese population.

AIMS: Visfatin is a newly discovered adipokine found in abundance in visceral fat. It lowers plasma glucose in humans and mice. In this study, we explored the relationships between the plasma level of visfatin and genetic single nucleotide polymorphisms (SNPs) and Type 2 diabetes mellitus (T2DM) and anthropometric and metabolic parameters in Chinese subjects. METHODS: Oral glucose tolerance tests (OGTT) and biochemical assays for plasma insulin, lipid profiles and serum visfatin were performed in 241 newly diagnosed T2DM patients, subjects with impaired glucose regulation (IGR), and normal glucose tolerant subjects more than 40 years of age. Genotyping for three SNP loci: -1535C/T, rs2058539 and rs10953502 were performed using the allele-specific real-time PCR method. RESULTS: Visfatin levels were similar in T2DM patients, IGR and normal glucose tolerant subjects. However, visfatin levels were significantly lower in obese than normal-weight subjects (13.66 +/- 0.87 vs. 15.46 +/- 0.47 ng/ml, P = 0.03). There was suggestively significant correlation between visfatin level and body mass index (r = -0.17 P = 0.07) and waist-hip ratio (r = 0.16 P = 0.08) in male subjects, but not in female subjects. Allele and common haplotype frequencies of the three SNP loci were similar in T2DM patients, IGR and normal glucose tolerant subjects. However, significant associations were found between these three SNP loci and plasma glucose concentration at 0 and 120 min during OGTT, the area under the response curve for plasma glucose, and triglyceride and total cholesterol levels. CONCLUSIONS: Serum visfatin levels may be related to visceral obesity in men, and the visfatin gene may account for variation of glucose and lipid parameters in Chinese subjects.     

单纯性肥胖青少年血清内脂素水平及其与年龄和高密度脂蛋白胆固醇的关系

目的 检测单纯性肥胖及正常青少年血清内脂素水平,探讨其与年龄、体重指数(BMI)、脂联素、瘦素、血脂、血糖及胰岛素水平的关系.方法 研究对象共148名,其中单纯性肥胖症青少年72例,正常对照76名.采用放射免疫分析法、酶法测定两组青少年的空腹血清内脂素、脂联素、瘦素、睾酮、甘油三酯、总胆固醇、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇(HDL-C)等.肥胖组青少年均做口服葡萄糖耐量试验(OGTF),计算胰岛素抵抗指数(HOMA-IR)、胰岛素敏感指数(ISI)和早期胰岛素分泌指数(EISI).结果 肥胖组血清内脂素水平显著高于正常对照组[(37.65±18.28 vs 29.35±12.10) μg/L,P<0.01].正常对照组血清内脂素水平与人体测量指数及脂质参数之间无任何相关性,而肥胖组血清内脂素与年龄、EISI和Tanner分期呈负相关,与血清HDL-C水平呈正相关.并且在校正年龄、性别、体重指数后,内脂素水平与年龄及HDL-C水平仍然呈显著相关(g<0.05).结论 在中国青少年人群中,血清内脂素随年龄增长而下降,且可能参与体内HDL-C代谢的调控.     

Serum visfatin concentrations in obese adolescents and its correlation with age and high-density lipoprotein cholesterol

Visfatin was recently identified as an adipocytokine and has insulin mimetic properties, but its role in adolescents remains largely unknown. In this study, we examined the impact of adolescent obesity on circulating visfatin levels and the relationship between visfatin and anthropometric indices, insulin sensitivity, and blood lipids in Chinese adolescents (11-18 years). Serum visfatin, adiponectin, leptin, and blood lipids were measured in 76 non-obese and 72 obese adolescents. The medians of serum visfatin levels were significantly higher in obese subjects of 34.68ng/ml than in non-obese subjects of 28.67ng/ml (P=0.002). There were no significant correlations in the non-obese group between the serum visfatin concentration and the anthropometric indices or the lipid parameters. However, visfatin levels were negatively correlated with age, early insulin secretion index (EISI), Tanner stage, and positively correlated with HDL-c in the obese adolescents. These relationships, except that for EISI and Tanner stage, remained significant (P<0.05) after adjusting for age, gender, and body mass index. Moreover, unlike adiponectin and leptin, visfatin concentration did not correlate with testosterone in non-obese and obese boys. In conclusion, visfatin levels may decrease with age and be related to the HDL metabolism in obese adolescents.     

Serum concentration of visfatin in obese women

The aim of the present study was to determine serum concentrations of visfatin in obese women in comparison to normal-weight controls. Study subjects were 21 obese women without additional disease (age, 29.0+/-4.9 years; body mass index, 37.1+/-6.1 kg/m2) and 16 healthy, normal-weight women (age, 29.9+/-5.4 years; body mass index, 22.5+/-1.7 kg/m2). Body composition was measured by bioimpedance. Serum concentrations of visfatin were assayed with an enzyme-linked immunosorbent assay kit (Phoenix Pharmaceuticals, Burlingame, CA). Insulin was determined by radioimmunoassay and glucose by colorimetric method. Serum concentration of visfatin was significantly higher in obese women when compared to controls. Positive correlations between serum concentrations of visfatin and insulin in the obese group were found. In the control group, we observed positive correlations between serum concentrations of visfatin and glucose. In conclusion, the observed increase of visfatin in obesity may be a counterregulation preventing further glucose increase.     

Serum visfatin levels, adiposity and glucose metabolism in obese adolescents

Objective: Visfatin, an adipokine, has insulin-mimetic effects. The main determinants of both the production and the physiologic role of visfatin are still unclear. The aim of this study is to determine the relation of serum visfatin to adiposity and glucose metabolism.Methods: 40 pubertal adolescents (20 females, 20 males; age range: 9-17 years) with exogenous obesity and 20 age- and sex-matched healthy adolescents (10 females, 10 males) were enrolled in the study. Oral glucose tolerance test (OGTT) was performed in the obese group. Serum glucose, insulin and visfatin levels were analyzed in the fasting state in the controls and at 0, 60 and 120 minutes during the OGTT in the obese group.Results: The obese group had higher serum visfatin levels than the control group [11.6 (3.3-26) ng/mL vs. 7.5 (3.3-10.5) ng/mL, p<0.001]. Visfatin levels were correlated positively with body mass index, waist/hip ratio, insulin, and homeostasis model assessment for insulin resistance and negatively with glucose/insulin ratio in the combined group (obese subjects plus controls). Visfatin levels were essentially similar in obese subjects with and without insulin resistance (p>0.05). Serum visfatin levels did not change at 60 and 120 minutes of the OGTT compared to the baseline levels (p>0.05).Conclusions: Serum visfatin levels are elevated in obese adolescents and do not change with acute changes in glucose metabolism. Visfatin levels are related with adiposity and glucose metabolism parameters. However, the role and contribution of adiposity and glucose metabolism to the circulating visfatin levels in obese patients remain to be explored. Conflict of interest:None declared.