不同强度运动结合白藜芦醇对老年肥胖大鼠RBP4的影响

目的：探讨不同强度运动结合白藜芦醇对老年肥胖大鼠内脏脂肪组织视黄醇结合蛋白4（RBP4） mRNA蛋白表达及血浆RBP4浓度的影响。方法：选择鼠龄3周的雄性SD大鼠80只,随机分为对照组和实验组：对照组（C）饲喂6.0%脂肪的普通饲料（n=12）;实验组分3个阶段饲喂36%~40%高脂饲料（n=68）。建立老年肥胖大鼠模型,选取24只建模成功的肥胖大鼠随机分为4组（n=6）：肥胖对照组（CO）、白藜芦醇组（RO）、低强度运动+白藜芦醇组（LRO）、中强度运动+白藜芦醇组（MRO）。LRO组和MRO组的运动强度分别为（12 m/min×15 min）和（15 m/min×15 min）,每天运动60 min;补充白藜芦醇各组52.5 mg/kg·d灌胃1次,对照组采用等量的纯净水灌胃,持续干预8周。8周后采血和肾周、睾周、血管及内脏脂肪组织,检测血糖和血浆RBP4浓度、计算胰岛素敏感性（ISI）,检测RBP4 mRNA和蛋白表达。结果：与正常组比较,模型组大鼠RBP4 mRNA和蛋白表达、血浆浓度及血糖指标明显升高（P<0.05,P<0.01）,ISI明显降低（P<0.05）;与模型组比较,RO、LRO组和MRO组大鼠RBP4 mRNA和蛋白表达、血浆浓度及血糖指标明显降低（P<0.05,P<0.01）,ISI明显升高（P<0.05）;RO、LRO组和MRO组之间比较,MRO组大鼠RBP4 mRNA和蛋白表达、血浆浓度及血糖指标明显降低,ISI明显升高,但无显著差异。结论：不同强度运动结合白藜芦醇能降低老年肥胖大鼠内脏脂肪组织RBP4 mRNA和蛋白表达及血浆RBP4浓度,受运动强度影响较小。     

运动结合甲鱼油对老年肥胖大鼠chemerin的影响

目的：探讨运动结合甲鱼油对老年肥胖大鼠脂肪因子chemerin的影响。方法：选取雄性SD大鼠50只,鼠龄3周,随机分为对照组（n=12）和实验组（n=32）,对照组喂食普通饲料,实验组喂食高脂饲料。鼠龄达到60周后,随机选取喂食普通饲料的6只大鼠为对照组（C组）;随机选取喂食高脂饲料、体重大于对照组平均体重120%的大鼠24只,随机分为4组（n=6）：肥胖对照组（OC）、运动组（OE）、甲鱼油组（TO）、运动结合甲鱼油组（OET）。干预方案为：大鼠跑台运动,坡度0°、速度15 m/min,每组15 min、4组/次,组间休息5 min;甲鱼油灌胃0.3~0.4 ml/次,每日一次,5次/周,干预持续8周。8周后,检测内脏脂肪组织chemerin mRNA和蛋白表达以及血浆chemerin浓度,测定血糖和胰岛素浓度,计算胰岛素敏感性指数。结果：干预8周后,OE和TO组的chemerin蛋白表达明显低于OC组（P< 0.05）,OET组的chemerin蛋白表达则明显低于OC、OE、TO组（P<0.01）;OC组血浆c hemer in浓度明显高于C组（P<0.01）,TO、OE和OET组血浆chemerin浓度均明显低于OC组（P<0.05,P<0.01）;OC组血糖水平显著高于C组（P<0.01）,OE、TO、OET组血糖水平均明显低于OC组（P<0.05）;OC组胰岛素敏感性指数明显低于C组（P<0.05）,OE、TO和OET组胰岛素敏感性指数则显著高于OC组（P<0.05,P<0.01）。结论：老年肥胖大鼠血浆chemerin浓度及血糖水平增高,胰岛素敏感性降低;运动结合甲鱼油能明显降低老年肥胖大鼠内脏脂肪组织chem erin蛋白质表达,降低血浆chemerin浓度及血糖水平,提高胰岛素敏感性。推测运动结合甲鱼油干预可能是改善老年肥胖和预防肥胖相关疾病的有效手段。     

脂肪因子Vaspin在运动与甲鱼油对老年肥胖大鼠胰岛素抵抗的作用*

目的: 从Vaspin在内脏脂肪组织mRNA表达、蛋白表达以及血浆浓度角度,探讨Vaspin在运动结合甲鱼油对老年肥胖大鼠胰岛素抵抗(IR)的调节作用。方法: 选取鼠龄3周的雄性SD大鼠(n=50),持续喂普通饲料至大鼠55周龄,根据体重无差异选取38只喂饲高脂饲料(脂肪含量占40%),建立老年肥胖模型,喂饲至大鼠周龄60周。建模成功后,随机选取24只分为4组(n=6),分别为肥胖模型组(OA)、运动组(OB)、单纯补充甲鱼油组(OF)、运动结合甲鱼油组(OBF)。(运动)干预方案:大鼠运动跑台坡度为0°、速度和时间(15 m/min,15 min)、组间休息5 min、4组/次,甲鱼油灌胃0.3～0.4 ml,1次/天,其他组灌胃相等剂量的生理盐水,5次/周,持续8周。8周后,取血测定大鼠血糖、血浆胰岛素和Vaspin浓度,取肾和睾丸周围内脏脂肪组织,检测脂肪组织Vaspin mRNA及蛋白的表达。结果: 与肥胖模型组相比,8周干预后,OB、OF和OBF组的血糖水平明显降低(P＜0.05,P＜0.01),OB和OBF组的血浆Vaspin浓度明显降低(P＜0.05,P＜0.01),血浆胰岛素浓度无明显变化,OB、OF和OBF组的IR、内脏脂肪组织中Vaspin mRNA和蛋白表达均明显降低(P＜0.01);与OBF组相比,OB和OF组的血糖、IR、血浆Vaspin浓度、内脏脂肪组织中Vaspin mRNA和蛋白表达各组间均无统计学意义(P＞0.05)。结论: 运动与甲鱼油均可以改善老年肥胖大鼠IR、降低血糖,伴随着内脏脂肪Vaspin mRNA表达、蛋白表达及其血浆浓度降低,但运动结合甲鱼油并不能取得更好的协同效果。     

高脂饲料诱导的肥胖大鼠网膜素水平的实验研究

人群调查发现肥胖人群网膜素水平较正常人群低,而正常及肥胖大鼠血清网膜素水平及其基因表达情况尚不清楚.将SD大鼠随机分为正常组(n=10)和高脂组(n=30),分别喂养普通饲料和高脂饲料.6 w后从高脂组选取体重增长最快的20只,再从中随机抽取10只继续喂养高脂饲料,12 w后两组各剩9只,采用全自动生化仪ADVIA2400测定血糖及血脂、ELISA检测血清胰岛素及网膜素水平、RT-PCR检测网膜脂肪组织网膜素mRNA表达水平.结果显示高脂组大鼠体重、体重增加值、肥胖指数、低密度脂蛋白、胰岛素、血清网膜素水平及网膜脂肪组织网膜素mRNA表达水平均高于正常组(P<0.05).首次发现肥胖大鼠血清网膜素水平及网膜脂肪组织中网膜素mRNA表达水平较正常大鼠显著增高,与人群调查结果不一致.     

脂联素与胰岛素抵抗研究进展

脂联素是脂肪组织分泌一种脂肪因子,与胰岛素抵抗和肥胖密切相关,在2型糖尿病和肥胖人群中,脂联素的血浆浓度下降。脂联素信号通路通过激活AMPK和PPAR-α与胰岛素信号通路相联系。研究表明,上调脂联素信号通路的活性可以有效缓解胰岛素抵抗。因此,脂联素信号转导通路机制是以胰岛素抵抗为病理生理基础的2型糖尿病的研究热点。本文简要介绍脂联素的生物学特征、脂联素的信号通路机制、脂联素与胰岛素抵抗的现有研究成果及临床价值。     

高脂饮食诱导的C57BL／6J肥胖小鼠脂肪组织RIP140基因表达水平的研究

目的：探讨高脂饮食致肥胖小鼠脂肪组织RIP140mRNA表达水平的变化及其与胰岛素抵抗的关系。方法：将C57BL／6J雄性小鼠随机分为正常饮食（NFD）组、高脂饮食（HFD）纽分别喂养14周后,测量两组小鼠体重,以NFD组小鼠体重作为对照,选取HFD组中体重大于对照组小鼠平均体重20％的小鼠作为肥胖组小鼠。对照组和肥胖组小鼠取血测甘油三酯（TG）、总胆固醇（TC）、空腹血糖（FBG）、空腹胰岛素水平（FIns）,计算稳态模型胰岛素抵抗指数（HOMA-IR）;采用RT—PCR技术检测两组小鼠附睾脂肪组织RIP140 mRNA的表达水平,并进行统计学分析。结果：HDF组小鼠中有12只符合标准计入肥胖组。肥胖组小鼠TG、TC、FBG、Fins（P〈0．05）,HOMA-1R（P〈0．01）均明显高于对照组;肥胖组小鼠脂肪组织RIP140mRNA的表达高于对照组,差异具有统计学意义（P〈0．05）;相关分析显示小鼠脂肪组织R1P140 mRNA表达水平与TG水平呈正相关（r=0．536,P〈0．05）,与胰岛素抵抗指数呈正相关（r=0．465,P〈0．05）,而与TC、FBG、Fins水平相关分析无统计学意义（P〉0．05）。结论：高脂饮食诱导的肥胖小鼠脂肪组织RIP140 mRNA表达增加,并与胰岛素抵抗程度呈正相关。     

高脂饮食诱导的C57BL/6J肥胖小鼠脂肪组织RIP140基因表达水平的研究(英文)

目的:探讨高脂饮食致肥胖小鼠脂肪组织RIP140mRNA表达水平的变化及其与胰岛素抵抗的关系。方法:将C57BL/6J雄性小鼠随机分为正常饮食(NFD)组、高脂饮食(HFD)组分别喂养14周后,测量两组小鼠体重,以NFD组小鼠体重作为对照,选取HFD组中体重大于对照组小鼠平均体重20%的小鼠作为肥胖组小鼠。对照组和肥胖组小鼠取血测甘油三酯(TG)、总胆固醇(TC)、空腹血糖(FBG)、空腹胰岛素水平(FIns),计算稳态模型胰岛素抵抗指数(HOMA-IR);采用RT-PCR技术检测两组小鼠附睾脂肪组织RIP140 mRNA的表达水平,并进行统计学分析。结果:HDF组小鼠中有12只符合标准计入肥胖组。肥胖组小鼠TG、TC、FBG、FIns(P0.05),HOMA-IR(P0.01)均明显高于对照组;肥胖组小鼠脂肪组织RIP140 mRNA的表达高于对照组,差异具有统计学意义(P0.05);相关分析显示小鼠脂肪组织RIP140 mRNA表达水平与TG水平呈正相关(r=0.536,P0.05),与胰岛素抵抗指数呈正相关(r=0.465,P0.05),而与TC、FBG、FIns水平相关分析无统计学意义(P0.05)。结论:高脂饮食诱导的肥胖小鼠脂肪组织RIP140 mRNA表达增加,并与胰岛素抵抗程度呈正相关。     

饮食诱导肥胖及肥胖抵抗与脂肪细胞因子

Levin提出饮食诱导肥胖（DIO）与饮食诱导肥胖抵抗（DIO-R）的概念后,其发生机制受到了广泛关注。现代研究认为脂肪组织除了能调节能量代谢外,还可以分泌多种细胞因子,如瘦素、脂联素、肿瘤坏死因子-α（TNF-α）和抵抗素等。在已发现的脂肪细胞因子中,瘦素、TNF-α和脂联素等与肥胖的发生密切关联。DIO大鼠血清瘦素水平比DIO-R大鼠高,DIO大鼠瘦素敏感性降低,发生了瘦素抵抗。DIO小鼠血浆脂联素水平比DIO-R小鼠低。DIO组TNF-α水平明显高于DIO-R组。     

褪黑素受体激动剂改善高糖高脂喂养大鼠脂联素敏感性

目的观察褪黑素受体激动剂（NEU-P11）对高糖高脂饲养大鼠脂联素敏感性的影响。方法将30只SD大鼠随机分为对照组（CD组）,高糖高脂组（HFSD组）,褪黑素组（Mel组）,褪黑素受体激动剂组（NEU-P11组）。CD组饲以正常饲料;其余3组饲以高糖高脂饲料。6个月后,给药治疗2个月。治疗期间,Mel组每天注射Mel（4mg／kg）;NEU—P11组每天注射NEU-P11（10mg／kg）;CD组以及HFSD组注射生理盐水（5ml／kg）。测定糖脂代谢指标并做口服葡萄糖耐量实验（oral glucose tolerant test,OG-TY）,Western印迹检测脂联素（adiponectin,APN）在脂肪组织及脂联素受体（AdipoR）在骨骼肌组织中的表达变化。结果高糖高脂饮食可诱导SD大鼠产生胰岛素抵抗,脂联素表达增加。Neu-P11治疗后,胰岛素敏感性增强．脂联素表达降低至正常水平。结论Neu-P11能提高胰岛素敏感性,改善脂联素抵抗。     

Visfatin mRNA在PCOS患者网膜脂肪组织中的表达

目的：探讨visfatin基因在多囊卵巢综合征（PCOS）网膜脂肪组织中的表达及相关影响因素。方法：采用半定量RT-PCR方法检测PCOS组（30例）和对照组（25例）网膜脂肪组织visfatin mRNA表达,并测量体重指数、腰臀比、空腹血糖、空腹胰岛素、胰岛素抵抗指数和血清性激素水平。结果：①PCOS组网膜脂肪组织visfatin mRNA表达量高于对照组（P=0.000）。②网膜脂肪组织visfatin mRNA的表达量与BMI、WHR、FINS、HOMA-IR呈正相关（P〈0.05）。③多元逐步回归分析显示,HOMA-IR（P=0.000）和WHR（P=0.005）是影响网膜脂肪组织visfatin mRNA表达的相关因素。结论：网膜脂肪组织visfatin mRNA表达可能与PCOS胰岛素抵抗的发生和肥胖相关。     

Differential patterns of serum concentration and adipose tissue expression of chemerin in obesity: Adipose depot specificity and gender dimorphism

Chemerin, a recognized chemoattractant, is expressed in adipose tissue and plays a role in adipocytes differentiation and metabolism. Gender- and adipose tissue-specific differences in human chemerin expression have not been well characterized. Therefore, these differences were assessed in the present study. The body mass index (BMI) and the circulating levels of chemerin and other inflammatory, adiposity and insulin resistance markers were assessed in female and male adults of varying degree of obesity. Chemerin mRNA expression was also measured in paired subcutaneous and visceral adipose tissue samples obtained from a subset of the study subjects. Serum chemerin concentrations correlated positively with BMI and serum leptin levels and negatively with high density lipoprotein (HDL)-cholesterol levels. No correlation was found between serum chemerin concentrations and fasting glucose, total cholesterol, low density lipoprotein (LDL)-cholesterol, triglycerides, insulin, C-reactive protein or adiponectin. Similarly, no relation was observed with the homeostasis model assessment for insulin resistance (HOMA-IR) values. Gender- and adipose tissue-specific differences were observed in chemerin mRNA expression levels, with expression significantly higher in women than men and in subcutaneous than visceral adipose tissue. Interestingly, we found a significant negative correlation between circulating chemerin levels and chemerin mRNA expression in subcutaneous fat. Among the subjects studied, circulating chemerin levels were associated with obesity markers but not with markers of insulin resistance. At the tissue level, fat depot-specific differential regulation of chemerin mRNA expression might contribute to the distinctive roles of subcutaneous vs. visceral adipose tissue in human obesity.     

Vaspin gene expression in human adipose tissue: association with obesity and type 2 diabetes

Recently, vaspin was identified as an adipokine with insulin-sensitizing effects, which is predominantly secreted from visceral adipose tissue in a rat model of type 2 diabetes. In this study, we examined whether vaspin mRNA expression is a marker of visceral obesity and correlates with anthropometric and metabolic parameters in paired samples of visceral and subcutaneous adipose tissue from 196 subjects with a wide range of obesity, body fat distribution, insulin sensitivity, and glucose tolerance. Vaspin mRNA expression was only detectable in 23% of the visceral and in 15% of the subcutaneous (SC) adipose tissue samples. Vaspin mRNA expression was not detectable in lean subjects (BMI<25) and was more frequently detected in patients with type 2 diabetes. No significant correlations were found between visceral vaspin gene expression and visceral fat area or SC vaspin expression. However, visceral vaspin expression significantly correlates with BMI, % body fat, and 2 h OGTT plasma glucose. Subcutaneous vaspin mRNA expression is significantly correlated with WHR, fasting plasma insulin concentration, and glucose infusion rate during steady state of an euglycemic-hyperinsulinemic clamp. Multivariate linear regression analysis revealed % body fat as strongest predictor of visceral vaspin and insulin sensitivity as strongest determinant of SC vaspin mRNA expression. In conclusion, our data indicate that induction of human vaspin mRNA expression in adipose tissue is regulated in a fat depot-specific manner and could be associated with parameters of obesity, insulin resistance, and glucose metabolism.     

有氧运动同时补充玉米肽对肥胖大鼠脂肪分解关键酶的影响

目的：研究有氧运动同时补充玉米肽对高脂饮食诱导的肥胖大鼠减脂的作用及其与脂肪分解关键酶甘油三酯脂肪酶（ATGL）和脂蛋白酯酶（LPL）关系。方法：4周龄健康雄性SD大鼠150只,体重160~180 g,随机选取15只作为普通膳食不运动组,给予普通饲料喂养。剩余135只大鼠进行8周的高脂饲料喂养建立肥胖大鼠模型,以体重超过普通膳食不运动组大鼠平均体重的20%作为肥胖大鼠建模成功的标准。将建模成功的肥胖大鼠40只随机分为5组（n=8）：肥胖对照组、酪蛋白组、玉米肽组、运动组和运动+玉米肽组。除酪蛋白组、玉米肽组喂养自制饲料外,其余各组均用普通饲料喂养,运动组每天进行15 m/min,持续时间60 min的跑台运动,每周6天。4周运动和玉米肽干预后取血,检测大鼠血浆中TG、TC、HDL、LDL的含量;取大鼠肾周、附睾脂肪和肝,检测肾周和附睾脂肪的重量,Western blot检测大鼠肝ATGL、脂肪LPL的蛋白表达水平。结果：与肥胖对照组大鼠相比：①运动组、运动+玉米肽组大鼠的体重、附睾和肾周脂肪含量明显降低（P<0.05）,且运动+玉米肽组比运动组下降得更明显（P<0.05）,而其它组大鼠无显著差异。②运动组大鼠血浆TG显著降低,运动+玉米肽组的血浆TG、TC显著降低（P<0.05）,其它组大鼠的TG、TC无显著差异;血浆HDL和LDL各组间均无显著性差异。③运动组和运动+玉米肽组大鼠的肝ATGL、脂肪组织LPL的蛋白水平明显增加（P<0.01）,且运动+玉米肽组比运动组的更显著（P<0.05）;其他两组无显著差异。结论：有氧运动、有氧运动同时补充玉米肽都可以明显降低大鼠的体脂和血脂水平,且后者的作用更强,这可能与其更显著地增加肥胖大鼠肝ATGL和脂肪LPL的蛋白水平有关。而仅仅补充玉米肽不能降低大鼠的体脂和血脂水平。     

Angiotensin II Receptor Blocker Ameliorates Stress-Induced Adipose Tissue Inflammation and Insulin Resistance

A strong causal link exists between psychological stress and insulin resistance as well with hypertension. Meanwhile, stress-related responses play critical roles in glucose metabolism in hypertensive patients. As clinical trials suggest that angiotensin-receptor blocker delays the onset of diabetes in hypertensive patients, we investigated the effects of irbesartan on stress-induced adipose tissue inflammation and insulin resistance. C57BL/6J mice were subjected to 2-week intermittent restraint stress and orally treated with vehicle, 3 and 10 mg/kg/day irbesartan. The plasma concentrations of lipid and proinflammatory cytokines [Monocyte Chemoattractant Protein-1 (MCP-1), tumor necrosis factor-α, and interleukin-6] were assessed with enzyme-linked immunosorbent assay. Monocyte/macrophage accumulation in inguinal white adipose tissue (WAT) was observed with CD11b-positive cell counts and mRNA expressions of CD68 and F4/80 using immunohistochemistry and RT-PCR methods respectively. The mRNA levels of angiotensinogen, proinflammatory cytokines shown above, and adiponectin in WAT were also assessed with RT-PCR method. Glucose metabolism was assessed by glucose tolerance tests (GTTs) and insulin tolerance tests, and mRNA expression of insulin receptor substrate-1 (IRS-1) and glucose transporter 4 (GLUT4) in WAT. Restraint stress increased monocyte accumulation, plasma free fatty acids, expression of angiotensinogen and proinflammatory cytokines including MCP-1, and reduced adiponectin. Irbesartan reduced stress-induced monocyte accumulation in WAT in a dose dependent manner. Irbesartan treatment also suppressed induction of adipose angiotensinogen and proinflammatory cytokines in WAT and blood, and reversed changes in adiponectin expression. Notably, irbesartan suppressed stress-induced reduction in adipose tissue weight and free fatty acid release, and improved insulin tolerance with restoration of IRS-1 and GLUT4 mRNA expressions in WAT. The results indicate that irbesartan improves stress-induced adipose tissue inflammation and insulin resistance. Our results suggests that irbesartan treatment exerts additive benefits for glucose metabolism in hypertensive patients with mental stress.     

内脏脂肪组织沉默信息调节因子1在高脂诱导西藏小型猪胰岛素抵抗中的表达研究*

目的: 探讨内脏脂肪组织沉默信息调节因子1(Sirt1)在高脂诱导西藏小型猪肥胖和胰岛素抵抗中的表达。方法: 12只雄性西藏小型猪,随机分为正常对照组(NC)和高脂组(HFC),每组6只。造模16周后,测量空腹体重、体质量指数(BMI),并取前腔静脉血,测量总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)和高密度脂蛋白胆固醇(HDL-C),计算动脉硬化指数(AI);同时,进行静脉糖耐量实验。在动物进行安乐死后,检测内脏脂肪率,并取内脏脂肪组织进行病理组织学观察和脂肪细胞直径大小分析,并采用RT-PCR法观察脂肪组织中Sirt1、胰岛素样生长因子-1(IGF-1)、葡萄糖转运蛋白4(GLUT4)、过氧化物酶体增殖物激活受体γ(PPARγ)、过氧化物酶体增殖活化受体γ辅助活化因子1α(PGC-1α)、叉头框蛋白O1(FoxO1)、脂肪分解相关基因激素敏感性脂肪酶(HSL)及脂肪合成相关基因脂肪酸合成酶(FASN)的mRNA水平变化。结果: 与NC组比较,HFC组体重、BMI指数、TC、LDL-C、HDL-C、AI和内脏脂肪率均显著升高(P＜0.05,P＜0.01);同时,糖耐量曲线明显延迟并且血糖和胰岛素曲线下面积均显著升高(P＜0.05);HE病理观察和定量分析显示,脂肪细胞肥大且平均细胞直径明显增加(P＜0.01);另外,脂肪组织中Sirt1、PGC-1α 、GLUT4、HSL mRNA水平均有不同程度的降低,其中Sirt1和HSL mRNA表达显著降低(P ＜0.05),FOXO1、IGF-1、PPAR-γ和FASN mRNA表达则显著升高(P＜0.05, P＜0.01)。结论: 高脂饮食诱导西藏小型猪能形成肥胖模型,并具有脂质紊乱和胰岛素抵抗等表型特征;而Sirt1在内脏脂肪沉积和胰岛素敏感性降低中起着关键作用。     

Vaspin gene in rat adipose tissue: relation to obesity-induced insulin resistance

Visceral adipose fat has been claimed to be the link between obesity and insulin resistance through the released adipokines. This study aimed to assess the expression of vaspin as one of the recent adipokines in rats abdominal subcutaneous and visceral fat in diet-induced obese (DIO) and in DIO performing 3 weeks swimming exercise (DIO + EXE) compared to control and control + exercise (C + EXE) groups. Vaspin mRNA and protein expression assessed using RT-PCR and Western blotting analysis revealed vaspin expression in DIO and DIO + EXE but not in controls groups. In DIO group, visceral vaspin expression was higher than in that of subcutaneous fat and was positively correlated with body weight. Upregulation of visceral vaspin expression in DIO was concomitant with the development of insulin resistance (increase in fasting serum insulin and HOMA-IR) and rise in serum leptin level. Unchanged visceral vaspin mRNA in DIO + EXE rats, with significant improvements of insulin resistance parameters and serum leptin compared to DIO group was found. In conclusion, increased visceral vaspin expression in obesity was associated with insulin resistance. Further investigations into the molecular links between vaspin and obesity may unravel innovative therapeutic strategies in people affected by obesity-linked insulin resistance, metabolic syndrome, and type 2 diabetes.     

TNF-alpha alters visfatin and adiponectin levels in human fat.

Adiponectin and visfatin are newly discovered adipokines that are strongly expressed in human visceral adipose tissue. To identify new regulatory mechanisms in fat, the effect of TNF-alpha (TNF) on adiponectin, on its two receptors, and on visfatin was investigated by incubating human visceral adipose tissue from patients without diabetes mellitus with TNF for 24, 48 and 72 hours. The mRNA expression of visfatin, adiponectin, and its two receptors, as well as the protein expression of adiponectin were determined. A decrease of adiponectin mRNA expression of 97% after incubation with TNF (5.75 nmol/l) for 24 hours, a decrease of 91% after 48 hours, and a decrease of 96% after 72 hours were measured. The reduction of protein expression was measured to be 42% after 24 hours, 28% after 48 hours, and 39% after 72 hours of incubation with TNF (5.75 nmol/l). The mRNA level of adiponectin receptor 1 (AdipoR1) was elevated about 72% after 48 hours of incubation and 67% after 72 hours of incubation, whereas the mRNA expression of adiponectin receptor 2 (AdipoR2) was not altered significantly. The visfatin mRNA level was found to be highly increased by 255% after 24 hours and 335% after 48 hours and 341% after 72 hours of incubation with TNF (5.75 nmol/l). Our results support the concept of visceral adipose tissue as an endocrine organ. We demonstrate that TNF has regulatory functions on adiponectin, AdipoR1 and on visfatin in human visceral adipose tissue. TNF levels are elevated in states of obesity and insulin resistance. Due to this fact TNF could be the reason that there is a decrease in the level of adiponectin, whereas there is an increase in the level of visfatin in states of obesity and insulin resistance.