PAQR9对棕色脂肪产热及UCP1表达的影响

目的 初步探究孕激素和脂联素受体家族成员9（progestin and adipoQ receptor family member 9,PAQR9）对棕色脂肪产热及解偶联蛋白1（uncoupling protein 1,UCP1）表达的影响。方法 选取C57BL/6J小鼠的白色脂肪组织（white adipose tissue,WAT）、棕色脂肪组织（brown adipose tissue,BAT）及前棕色脂肪细胞系DE2-3和间充质干细胞C3H10T1/2细胞系进行研究。实时荧光定量PCR技术检测不同条件下PAQR9及UCP1的mRNA水平,蛋白免疫印迹法检测UCP1的蛋白质水平。实时荧光定量PCR技术和油红O染色法检测脂肪细胞的成脂分化情况。结果 C57BL/6J小鼠BAT中PAQR9的mRNA水平显著高于WAT。冷刺激诱导下,BAT和腹股沟皮下WAT中PAQR9的mRNA水平显著升高。DE2-3细胞诱导分化成熟即第6天时,PAQR9的mRNA水平显著高表达。在DE2-3细胞中过表达PAQR9,UCP1的mRNA水平显著上调,细胞耗氧量显著增加,而DE2-3细胞成脂分化功能无显著性差异。在DE2-3细胞中敲低PAQR9,UCP1的mRNA水平显著下调。在C3H10T1/2细胞第4~6天脂肪细胞分化成熟时,PAQR9的mRNA水平显著上调,在敲低PAQR9后UCP1蛋白质水平下调,而C3H10T1/2细胞成脂分化功能无显著性差异。结论 PAQR9能够促进棕色脂肪细胞产热,调控产热基因UCP1的表达。     

Medium-Chain Triglyceride Activated Brown Adipose Tissue and Induced Reduction of Fat Mass in C57BL/6J Mice Fed High-fat Diet

Objective To investigate activation of brown adipose tissue (BAT) stimulated by medium-chain triglyceride (MCT). Methods 30 Male C57BL/6J obese mice induced by fed high fat diet (HFD) were divided into 2 groups, and fed another HFD with 2% MCT or long-chain triglyceride (LCT) respectively for 12 weeks. Body weight, blood biochemical variables, interscapular brown fat tissue (IBAT) mass, expressions of mRNA and protein of beta 3-adrenergic receptors (β3-AR), uncoupling protein-1 (UCP1), hormone sensitive lipase (HSL), protein kinase A (PKA), and adipose triglyceride lipase (ATGL) in IBAT were measured. Results Significant decrease in body weight and body fat mass was observed in MCT group as compared with LCT group (P<0.05) after 12 weeks. Greater increases in IBAT mass was observed in MCT group than in LCT group (P<0.05). Blood TG, TC, LDL-C in MCT group were decreased significantly, meanwhile blood HDL-C, ratio of HDL-C/LDL-C and norepinephrine were increased markedly. Expressions of mRNA and protein ofβ3-AR, UCP1, PKA, HSL, ATGL in BAT were greater in MCT group than in LCT group (P<0.05). Conclusion Our results suggest that MCT stimulated the activation of BAT, possible via norepinephrine pathway, which might partially contribute to reduction of the body fat mass in obese mice fed high fat diet.     

Anti-obesity Action of Fermented Barley Extracts with Lactobacillus plantarum dy-1 and Associated Micro RNA Expression in High-fat Diet-induced Obese Rats

Objective To further explore associated effects of Lactobacillus plantarum dy-1(LFBE) on obesity and lipid metabolism at the gene expression level, the expression of micro RNAs(mi RNAs) was investigated in the liver of high-fat diet(HFD) induced obese rats.Methods Three groups of animal models were established. Changes in mi RNA expression in the liver of each group were analyzed by microarray and RT-q PCR, complemented by bioinformatics. Palmitateinduced hepatocellular carcinoma(Hep G2) cells were used as a model to validate the test.Results LFBE treatment groups and HFD groups were observed to be distinctly different with respect to rates of increase in body weight and body fat percentage and triglyceride(TG) and total cholesterol(TC) levels in serum and liver. In addition, the LFBE group showed upregulation of ten mi RNAs and downregulation of five mi RNAs in the liver. Downregulation of mi R-34 a and mi R-212 was observed in the livers of the LFBE group. Gene ontology and kyoto encyelopedia of geues and genomes(KEGG)pathway analysis showed that possible target genes of the deregulated mi RNAs were significantly enriched in the adrenergic and HIF-1 signaling pathways.Conclusion These results demonstrate that LFBE might regulate the expression of mi RNAs in order to inhibit obesity and fatty liver.     

Effect of Acupuncture on Uncoupling Protein 1 Gene Expression for Brown Adipose Tissue of Obese Rats

Objective:To explore the effects of acupuncture on the expression of uncoupling protein 1(UCP_1)gene of brown adipose tissue (BAT)in obese rats.Methods:The expression of UCP_1 gene ofBAT was determined with RT-PCR technique.The changes of body weight,Lee’s index,body fat,andthe expression of UCP_1 gene of BAT in obese rats were observed before and after acupuncture.Results:The body weight,Lee’s indeX,body fat in obese rats were all markedly higher than those in normal rats,but the expression of UCP_1 gene of BAT in obese rats was all lower than that in normal rats.There werenegative correlation between the Obesity index and the expression of UCP_1 gent in BAT.After acupunc-ture the marked effect of weight loss was achieved while the expression of UCP_1 gene of BAT Obviously in-creased in obese rats.Conclusion:The abnormal reduction for expression of UCP_1 gene of BAT might bean important cause for the obesity.To promote the expression of UCP_1 in obese organism might be an im-portant cellular and mole     

匹格列酮对肥胖小鼠棕色脂肪功能的影响

目的:使用高脂饮食诱导(high fat diet-induced, HFD)的肥胖小鼠模型,研究过氧化物酶体增殖物激活受体γ(peroxisome proliferator-activated receptor γ,PPARγ)激动剂匹格列酮(pioglitazone,PGZ)对肥胖小鼠棕色脂肪组织功能的影响,及可能的作用机制?方法:建立HFD肥胖小鼠模型(n=30);肥胖小鼠随机分为PGZ灌胃组和对照组(每组15只),PGZ 10 mg/(kg·d)灌胃1个月,对照组使用等量生理盐水灌胃?检测灌胃组及对照组小鼠的体重?口服葡萄糖耐量(OGTT)?血胰岛素含量;使用RT-PCR检测小鼠棕色脂肪组织特异性基因表达;使用Western blot检测小鼠棕色脂肪组织UCP-1蛋白的表达量?结果:PGZ灌胃的肥胖小鼠棕色脂肪功能相关基因和蛋白表达提高;PGZ灌胃组小鼠体重?血胰岛素含量和口服葡萄糖耐量改善?结论:PGZ通过调节棕色脂肪功能基因表达提高棕色脂肪功能,可能是PGZ改善胰岛素抵抗和机体代谢的重要原因?     

高脂饮食诱导的肥胖小鼠中缺氧对胰岛素抵抗及脂肪组织巨噬细胞浸润的影响

 目的  研究缺氧在高脂饮食诱导的肥胖(diet-induced obesity,DIO)小鼠模型中对胰岛素抵抗及脂肪组织巨噬细胞浸润的影响。   方法  建立DIO小鼠模型,动态观察高脂饮食(high-fat diet,HFD)喂养小鼠4、8、12周时的体质量、白色脂肪(white adipose tissue,WAT)量及其与体质量的比值、空腹血糖、空腹胰岛素、糖耐量和胰岛素抵抗、脂肪组织中F4/80标记的巨噬细胞浸润,采用hypoxyprobeTM-1试剂盒(哌莫硝唑标记法)评价DIO小鼠的脂肪组织是否存在缺氧及其出现时间,分析缺氧与上述指标异常出现的时间先后,探讨缺氧在HFD致胰岛素抵抗、脂肪组织巨噬细胞浸润中的作用。  结果  DIO小鼠4周时即出现糖耐量异常,8周时出现胰岛素抵抗;WAT存在局部缺氧,与巨噬细胞浸润增加同步出现在HFD后12周时间点,迟于糖耐量异常和胰岛素抵抗的出现。  结论  缺氧可能不是DIO时糖代谢异常和胰岛素抵抗的启动因素。     

白色脂肪细胞棕色化:肥胖症及其相关代谢性疾病治疗的新靶点

棕色脂肪组织(BAT)在维持体温恒定和调节能量代谢方面发挥着重要的生理作用。近年来研究发现,寒冷刺激可促进成人体内出现棕色样脂肪细胞,这种脂肪细胞的基因表达谱介于白色脂肪细胞和经典的棕色脂肪细胞之间,于是提出了"白色脂肪细胞棕色化"的概念,且认为过氧化物酶体增殖物激活受体γ、肌肉抑制素、成纤维细胞生长因子21、irisin等因子参与了这一过程。白色脂肪细胞棕色化后,能显著促进机体能量的消耗,改善机体糖脂代谢,因此,可能成为针对肥胖症及其相关代谢异常疾病治疗的新靶点。     

脂肪组织在CYP1B1缺失保护小鼠营养性肥胖中的作用

目的:从脂肪组织脂肪代谢和相关内分泌功能方面探讨CYP1B1在成年小鼠营养性肥胖中的作用.方法:CYP1B1基因敲除和野生型雄性6周龄小鼠各16只,给予低、高脂饲料共6周.处理结束后分离脂肪组织,采用实时荧光定量PCR技术测定脂肪组织中相关因子表达水平,免疫印记检测葡萄糖转运蛋白4(GLUT4)表达.结果:与野生高脂组比较,基因敲除高脂组小鼠体重增量低;荧光定量PCR结果显示,敲除高脂组小鼠白介素-6(IL-6)、血管生成素2、脂肪酸结合蛋白2(AP2)等基因表达分别是野生高脂组的0.42,0.36,0.29倍,血管生成素1基因表达是野生高脂组的1.76倍.结论:CYP1B1基因缺失,可能通过对脂肪组织脂肪代谢、炎症状态、血管新生等综合影响,改善营养性肥胖及胰岛素抵抗.     

ob／ob 与野生型小鼠脂肪组织的磁共振波谱研究

目的：探讨超高场强磁共振氢质子波谱（ hydrogen MR spectroscopy ,1 H-MRS）在全面评价ob/ob鼠及野生对照组小鼠白色脂肪组织和棕色脂肪脂质成分中的作用。方法：运用整体和单体素1 H-MRS方法对ob/ob及野生对照鼠进行活体波谱分析,整体1 H-MRS波谱定量全身脂质;单体素波谱计算白色和棕色脂肪的脂质含量,饱和及不饱和脂肪酸、双不饱和脂肪酸的相对含量及多聚不饱和程度。结果：整体1 H-MRS结果显示ob/ob鼠全身脂质含量显著高于野生型对照组,单体素1 H-MRS显示ob/ob鼠棕色脂肪脂质含量显著高于野生对照组,而两组鼠白色脂肪脂质含量的差异无统计学意义,ob/ob鼠白色脂肪的双不饱和脂肪酸及多聚不饱和程度均低于野生对照组。结论：1 H-MRS不仅可以定量白色和棕色脂肪的脂质含量,还可以分析其脂质成分。     

过氧化物酶增殖物激活受体γ激动剂对24例肥胖症患者米色脂肪细胞分化的影响

目的 探讨过氧化物酶增殖物激活受体γ(PPARγ)激动剂罗格列酮对肥胖症患者皮下白色脂肪组织的米色化的影响,为治疗肥胖症提供新的途径。 方法 选取择期手术的24例肥胖症患者皮下白色脂肪组织,分离脂肪组织基质细胞并进行成脂诱导分化,在诱导分化后期加入不同浓度的罗格列酮干预,根据干预方式的不同分为对照组、Rosi-1组(加入1 μmol/L罗格列酮)和Rosi-2组(加入2 μmol/L罗格列酮)。通过实时定量PCR法以及Western blotting法检测各组脂肪细胞中解偶联蛋白(UCP1)及米色脂肪细胞特异性产热基因的表达。通过比色法检测细胞培养液中甘油释放浓度来评估干预对脂肪细胞脂解功能的影响。 结果 加入罗格列酮干预后,Rosi-1组和Rosi-2组成熟脂肪细胞表现多脂滴外形,UCP1蛋白(t=23.12,P<0.01;t=7.35, P<0.01)和米色脂肪细胞特异性产热基因UCP1(t=2.63, P=0.03;t=9.86, P<0.01)、PPARγ(t=2.8, P=0.02;t=11.06, P<0.01)和PR16结构(PRDM16)基因(t=2.65, P=0.02;t=12.85, P<0.01)表达水平在Rosi-1组和Rosi-2组中均较对照组上调,且Rosi-1组(t=2.76, P=0.02)和Rosi-2组(t=5.83, P<0.01)的脂解能力较对照组增强。 结论 PPARγ激动剂可提高肥胖症患者白色脂肪组织的米色脂肪细胞的分化,从而促进白色脂肪组织的棕色化,选择性作用于脂肪组织的PPARγ激动剂的研发可以为肥胖症治疗提供新的途径。     

新生儿硬肿症患儿白色脂肪与棕色脂肪的脂肪酸组成、血清游离脂肪酸变化及其对血糖的影响

本文应用气相色谱法测定了新生儿患儿白色脂肪及棕色脂肪的脂肪酸百分含量和正常足月儿、早产儿、硬肿症及其它疾病患儿血清游离脂肪酸含量。结果表明白色脂肪中饱和脂肪酸含量高于不饱和脂肪酸,棕色脂肪则相反。棕色脂肪中亚油酸含量明显高于白色脂肪。文中分析了血清游离脂肪酸总量及各组分的变化和它们之间的关系,以及影响因素。还发现血清亚油酸与血糖之间有明显的正相关。     

间歇性低氧对大鼠解偶联蛋白2基因表达的影响

目的 探讨间歇性低氧对大鼠脂肪组织中解偶联蛋白2(UCP2)基因表达的影响.方法 将40只健康雄性SD大鼠随机分为4组,每组10只,分别置于模拟海拔4000米的常温、低氧氧舱中(0天、1天、7天和21天),每天8小时,应用半定量的逆转录-聚合酶链反应(RT-PCR)方法检测大鼠白色脂肪组织(WAT)中UCP2 mRNA的表达水平.结果 大鼠置于低氧环境21天后,其WAT中UCP2 mRNA的表达水平较其他3组显著降低.结论 随着低氧时间的延长,UCP2 mRNA的表达水平降低;UCP2 mRNA表达的降低可能是对间歇性低氧改变的一种适应性反应.     

中链甘油三酯对肥胖小鼠棕色脂肪及其β3肾上腺素能受体表达的影响

目的 观察中链甘油三酯对肥胖小鼠棕色脂肪中β 3肾上腺素能受体表达的影响.方法 复制高脂肪饲料肥胖小鼠模型,选取成功造模的小鼠30只,随机分为中链甘油三酯高脂组(MCT)和大豆油高脂组(LCT),每组15只,喂饲12周.观察研究前后各组小鼠体质量、体脂肪、血脂、棕色脂肪组织重量的差异以及棕色脂肪组织中β 3肾上腺素能受体mRNA表达水平的变化.结果 研究结束时,MCT组小鼠的体质量、体脂肪量显著低于LCT组(P＜0.05),血甘油三酯、总胆固醇、低密度脂蛋白胆固醇(LDL-C)浓度均显著低于LCT组(P＜0.05),高密度脂蛋白胆固醇(HDL-C)浓度以及HDL-C/LDL-C比值显著高于LCT组.MCT组棕色脂肪组织中环磷酸腺苷(cAMP)、蛋白激酶(PKA)及激素敏感脂酶(HSL)均显著高于LCT组.MCT组棕色脂肪组织重量及β 3肾上腺素能受体mRNA表达水平显著高于LCT组(P＜0.05).结论 MCT可促进棕色脂肪组织增殖及其β3肾上腺素能受体mRNA的表达.     

高原低氧对解偶联蛋白2mRNA表达的影响

目的探讨高原低氧对Wistar大鼠白色脂肪组织（White Adipose Tissue,WAT）解偶联蛋白2（Uncoupling Protein2,UCP2）mRNA表达的影响。方法将60只雄性Wistar大鼠随机分成6组,每组10只,分为对照组、低氧1天组、低氧3天组、低氧7天组、低氧15天组和低氧30天组。分别在西宁和可可西里地区（1天、3天、7天、15天和30天）采集WAT标本,应用半定量逆转录一聚合酶链式扩增反应（RT-PCR）方法检测UCP2mRNA的表达水平。结果低氧1天组、低氧3天组、低氧7天组、低氧15天组和低氧30天组的UCP2 mRNA表达水平降低,尤以30天组降低明显。血红蛋白值与UCP2 mRNA的表达呈较高的负相关。结论随着低氧时间的延长,UCP2mRNA的表达水平逐渐降低是对低氧环境的一种适应性反应。     

甲状腺激素对大鼠解偶联蛋白-2基因表达的影响

目的:探讨甲状腺激素对大鼠骨骼肌组织(SM)、肝组织(LV)和白色脂肪组织(WAT)中解偶联蛋白-2(UCP2)基因表达的影响。方法:正常雄性Wistar大鼠30只,随机分为对照组、甲状腺功能亢进(甲亢)组和甲状腺功能低下(甲低)组,应用左旋甲状腺素钠和甲巯咪唑造成大鼠甲亢和甲低状态;用放免法检测血清总T3、T4的浓度;用半定量逆转录聚合酶链反应(RT-PCR)检测SM、LV和WAT中UCP2mRNA的表达水平。结果:与对照组相比,甲亢组大鼠SM、LV和WAT中UCP2mRNA的水平分别增加了65%、50%和40%,甲低组大鼠SM、LV和WAT中UCP2mRNA的水平分别降低了9%、24%和20%,差异均具有统计学意义,P<0.05。结论:过量甲状腺激素对SM、LV和WAT中UCP2基因的表达具有上调作用,甲状腺激素水平过低则下调SM、LV和WAT中UCP2基因的表达。     

脾阳虚模型小鼠产热障碍机制及附子理中汤的干预作用

目的:研究附子理中汤对脾阳虚模型小鼠骨骼肌解偶联蛋白3(uncoupling protein3,UCP3)及其mRNA表达以及对骨骼肌能荷的影响。方法:小鼠随机分为4组,每组11只,取3组造模,剩下的1组作为正常组,对造模的3组贯序采取以下措施:施行肩胛骨棕色脂肪切除术;连续饲以高脂饲料28d;从造模的3组中取2组,每只鼠每天灌饲黄连解毒汤和附子理中汤,分别称为黄连组和附子组,均普通饮食和饮水,另外1组则为模型组,饲以高脂饲料和普通饮水,正常组作为对照组,普通饮食和饮水,第99天取左侧腓肠肌,测腓肠肌UCP3相对含量及其mRNA表达和肌能荷值。结果:附子组肌能荷值显著低于其他3组,和黄连组比较,差异有统计学意义(P<0.01),和模型组及对照组比较,差异有统计学意义(P<0.05),对照组和黄连组比较,差异有统计学意义(P<0.01),对照组和模型组比较,差异有统计学意义(P<0.05);附子组UCP3mRNA表达较高,各组和附子组比较,差异有统计学意义(P<0.01);黄连组UCP3相对含量较低,各组和黄连组比较,差异有统计学意义(P<0.05)。结论:脾阳虚动物产热障碍的部分机制可能在于骨骼肌UCP3含量降低、UCP3mRNA表达下调,使产热和产能过程失平衡,附子理中汤通过提高骨骼肌UCP3含量及其mRNA表达而发挥治疗效用。     

解耦联蛋白3的研究进展

在解耦联蛋白1(UCP1)的同源物解耦联蛋白3(UCP3)被克隆以后的13年中,人们对确定它的功能抱有浓厚的兴趣。尽管人们做了大量的工作,但是它的分子结构和生理生化功能还都没有真正弄清楚。基于它与UCP1高度同源,早期的研究是验证它的生热作用,但是有关这种作用的证据不足。目前的研究主要集中在两种假说上:UCP3减少活性氧簇产生,这样可阻止或减少氧化性破坏;UCP3从线粒体中输出脂肪酸阴离子或脂质过氧化产物。UCP3是老化、变性性疾病、癌症、肥胖、糖尿病和心力衰竭等的重要潜在治疗靶点。现就UCP3的结构、组织分布、功能及调节因素进行综述,并对其今后的研究方向进行展望。     

Fermented Barley Extracts with Lactobacillus plantarum dy-1 Rich in Vanillic Acid Modulate Glucose Consumption in Human HepG2 Cells

Objective To investigate the effect of fermented barley extracts with Lactobacillus plantarum dy-1(LFBE) for modulating glucose consumption in HepG2 cells via miR-212 regulation. Methods Hepatocellular carcinoma(HepG2) cells were treated with palmitate. After 12 h, palmitate-induced HepG2 cells were treated with LFBE and its main components. Changes in glucose consumption, proinflammatory cytokine secretion, and miRNA-212 expression in HepG2 cells was observed. Results Treatment with LFBE rich in vanillic acid(VA) increased glucose consumption and reduced proinflammatory cytokine secretion in HepG2 cells. LFBE and VA normalized the upregulation of miR-212, which led to the upregulation of dual-specificity phosphatase-9(DUSP9), a direct target of miR-212, at both protein and mR NA levels. Downregulation of miR-212 markedly increased glucose consumption and reduced proinflammatory cytokine secretion by enhancing DUSP9 expression. Conclusion The results showed the benefit of LFBE and miR-212 downregulation in modulating glucose consumption and reducing proinflammatory cytokine secretion by targeting DUSP9. VA in LFBE was a strong regulator of palmitate-induced abnormal glucose consumption in HepG2 cells and can be a primary mediator.     

外源性乳酸对高脂饲料诱导肥胖小鼠的代谢调节作用

探讨外源性乳酸对高脂喂养诱导肥胖小鼠的代谢调节作用。采用脂肪含量60%的全合成高脂饲料建立C57小鼠代谢紊乱及肥胖模型，一部分小鼠采取高脂饲料喂养4周造模，于造模同时腹腔注射给予500 mg/(kg·d) 乳酸预防性干预4周；另一部分小鼠采取高脂饲料喂养8周造模，于造模4周后给予500 mg/(kg·d) 乳酸治疗4周。试验期间测定各组小鼠体重、摄食量变化，检测血清葡萄糖、乳酸、甘油三酯、胰岛素及肝糖原水平，通过口服糖耐量（OGTT）和胰岛素耐量（ITT）检测机体葡萄糖代谢和胰岛素抵抗情况，实验结束解剖取脂肪组织称重并进行脂肪组织病理学检查，通过RT-PCR检测脂肪组织的脂质合成和脂质分解基因表达情况。结果显示:（1）4周预防给药试验中，乳酸对正常（CON）和高脂饮食（HFD）小鼠体重未见明显影响，却可提高皮下脂肪与内脏脂肪的质量比；乳酸给药可明显降低HFD小鼠空腹血糖和肝糖原，同时升高血乳酸水平，对HFD小鼠糖耐量受损具有显著改善；乳酸可改善HFD组脂肪细胞的大小和排列形态，同时明显下调脂肪组织中脂肪酸合成和脂解基因表达。（2）在治疗8周实验中，乳酸两种给药途径均能部分减轻HFD组小鼠和减少摄食量，对于脂肪质量有部分改善趋势；乳酸两种给药途径均可明显降低HFD小鼠空腹血糖，显著改善糖耐量和胰岛素耐量，对空腹胰岛素水平及胰岛素抵抗指数也有部分改善作用；乳酸两种给药途径对肥胖小鼠脂肪细胞形态有不同程度的改善作用，同时显著下调脂肪组织中脂解基因表达。由此可见，对于高脂饲料诱导的肥胖性代谢失衡小鼠，给予外源性乳酸可以刺激糖代谢，抑制脂肪组织脂解，避免脂肪细胞肥大，进而改善糖耐量和胰岛素敏感性，减轻糖脂代谢紊乱。     

Calorie control increased vaspin levels of serum and periepididymal adipose tissue in diet-induced obese rats in association with serum free fatty acid and tumor necrosis factor alpha

Background Vaspin was recently identified as a novel adipokine that is predominantly secreted from adipose tissue and exerts insulin-sensitizing effects. This study was undertaken to elucidate the regulative effects of calorie control on the expression of vaspin and its potential mechanism.Methods Diet-induced obese Sprague Dawley （SD） rats were adopted as experimental models and accepted interventions of various ingestions and pioglitazone. Various differentiated stages of cultured 3T3-L1 cells were dealt with pioglitazone or TNFα in vitro for 48 hours to further verify findings in animal experiments.Results The rats were successfully induced into an obese experimental model with hyperinsulinemia, hyperlipidemia, and increased serum free fatty acid and TNFa by 12-week high-fat diet. It was found that depending on whether the rats were fed by a high-fat diet or a basal diet, there was extremely higher vaspin in the periepididymal fat pad than in subcutaneous adipose tissues by 16 weeks. Vaspin in sera and the periepididymal fat pad was much lower in rats with a high-fat diet than those with a basal diet （all P 〈0.05）, but vaspin in subcutaneous fat tissues was prone to increase in rats with a high-fat diet. A 4-week calorie restriction or pioglitazone on the obese rats resulted in a partial recovery of vaspin levels in sera and periepididymal adipose tissues, especially the latter revealed a more obvious superiority and increased vaspin levels of subcutaneous adipose. Surprisingly, the treatment of 4-week high-fat diet on non-obese rats did not significantly depress vaspin of sera and periepididymal adipose tissues. However, it is unknown if re-feeding generated the effect on vaspin levels of obese and non-obese rats on sera or adipose tissues. The correlation analysis showed that vaspin levels of serum and periepididymal fat tissues were negatively correlated with serum FFA, TNFα and insulin; meanwhile, there was a positive correlation between serum vaspin and vaspin of periepididymal fat tissues. Pioglitazone enhanced vaspin levels in cultured 3T3-L1 cells and supernatant in various differentiated stages, and this effect became more and more obvious along with the change of preadipocytes into mature fat cells. Administration of TNFα caused suppression on vaspin expression in differentiated stages of 3T3-L1 cells.Conclusions The present data indicated that a long-term high-fat diet could induce obesity metabolic syndrome in SD rats and finally lead to lower vaspin of sera and periepididymal fat, while pioglitazone and chronic calorie-control ingestion could enhance the production of vaspin. It was undoubtedly demonstrated that vaspin expression was strongly associated with insulin sensitivity, serum FFA, and TNFα.