Comparative evaluation of the hypolipidemic effects of hydroxyethyl methylcellulose (HEMC) and hydroxypropyl methylcellulose (HPMC) in high fat-fed mice

The effect of hydroxyethyl methylcellulose (HEMC), in comparison with hydroxypropyl methylcellulose (HPMC), on the body weight and lipid metabolism in mice fed with high fat diet was investigated. The animals were given normal control diet (NC group), high fat diet (HF group), or high fat diet supplemented with either HEMC (HF+HEMC group) or HPMC (HF+HPMC group) for 6weeks. At the end of the experimental period, both HF+HEMC and HF+HPMC groups showed reduced body weight, body fat, plasma triglyceride and total cholesterol contents, atherogenic index and free fatty acid level, and increased HDL-cholesterol concentration relative to the HF group. The hypolipidemic effect was partly due to the inhibition of lipogenesis and regulation of adipokine production. These findings demonstrate that compared with HPMC, HEMC was similarly effective in improving the lipid metabolism under high fat diet condition and may be useful in the prevention and treatment of high fat diet-induced hyperlipidemia.     

机械加载对高脂饮食诱导的肥胖和非酒精性脂肪肝的治疗作用

目的 探讨机械加载对高脂饮食诱导的肥胖和非酒精性脂肪肝的疗效。方法 选用6周龄的C57BL/6雌性小鼠30只,体质量约18 g,按随机数字表法分为正常对照组（NC组）、高脂饮食组（HF组）和高脂饮食机械加载治疗组（HF+L组）,每组10只,持续饮食诱导12周。高脂饮食6周后,HF+L组进行机械加载治疗6周。实验动物进行体成分分析,观测全身体脂含量的变化。收集肾周脂肪、子宫周脂肪、肠系膜脂肪、腹股沟脂肪和肝脏并称量湿质量。留取部分肝脏做组织形态学检测,油红O和HE染色分析观察肝脏的病理改变,部分肝脏用于Western blot检测内质网应激相关蛋白（eIF2α、p-eIF2α、ATF4）的表达。结果 与NC组相比,高脂饮食导致HF组体质量、体脂明显增加,机械加载治疗后,HF+L组体质量、体脂较HF组明显降低（P＜0.05）。肝脏组织学结果表明,高脂饮食导致一定程度的肝脏脂肪变性,通过治疗后,脂肪变性得到有效缓解（P＜0.05）。Western blot分析结果表明,高脂饮食导致小鼠肝脏eIF2α、p-eIF2α和ATF4蛋白表达升高,机械加载能够抑制肝脏p-eIF2α和ATF4蛋白的表达。结论 机械加载能够有效缓解高脂饮食导致的体质量、体脂增加及非酒精性脂肪肝,其治疗作用可能与肝脏内质网应激有关。     

中度限食对肥胖小鼠胰岛β细胞分泌功能的影响

摘要： 目的 明确中度限食干预能否从形态和功能上逆转肥胖对胰岛β细胞的损伤。方法 4周龄雄性C57BL/6 小鼠喂以高脂饮食8周, 建立饮食诱导的肥胖模型, 随后进行3周的高脂转普食 （HF→NC组） 或在此基础上40%限食干预 （HF→NC CR组）, 同时设高脂对照组 （HF AL组） 和普食对照组 （NC AL组）, 每组20只。实验终点取胰腺组织行胰岛素免疫组化染色, 定量β细胞面积, 并行腹腔葡萄糖耐量试验及胰岛素耐量试验, 评估早时相和第二时相胰岛素分泌及胰岛素敏感性。同时, 分离小鼠胰岛, 行静态葡萄糖刺激的胰岛素分泌实验及胞浆胰岛素含量测定。结果 实验终点HF AL组表现为显著肥胖、 β细胞面积增加、 糖耐量受损、 早时相胰岛素分泌趋向降低及胰岛素抵抗, 同时离体胰岛实验显示胞浆胰岛素含量增加, 但胰岛素分泌缺陷： 基础胰岛素分泌升高了30.6%, 而16.7 mmol/L高糖刺激下的胰岛素分泌降低了52.1%。HF→NC组小鼠的糖耐量恢复正常, 体质量有所降低但未正常, 早时相胰岛素分泌及离体胰岛高糖刺激的胰岛素分泌较HF AL组并无改善。经过3周的限食干预, HF→NC CR组体质量、 β细胞面积、糖耐量、 早时相胰岛素分泌、 胰岛素敏感性及离体胰岛基础和高糖刺激下的胰岛素分泌均恢复正常。结论 中度（40%） 限食干预至体质量正常, 可逆转饮食诱导肥胖小鼠的胰岛β细胞分泌功能紊乱, 重建葡萄糖稳态。     

高脂诱导性肥胖大鼠的胰岛素敏感性与TNF-α及FFAs水平

目的观察正常大鼠在高脂饮食诱导下形成肥胖后的胰岛素敏感性及其TNF-α、FFAs的变化。方法9周龄健康雄性Wistar大鼠16只,随机分为正常饲养组(NC熏n=8)和高脂饲养组(HF熏n=8)。喂养10周,比较两组大鼠体重、胰岛素抵抗指数(HOMA-IR)、以及TNF-α、FFAs等的变化。结果经10周高脂喂养,HF组与NC组比较,体重和内脏脂肪组织显著增加(HF组大鼠体重较NC组增加了11.4%,P<0.05;HF组大鼠内脏脂肪组织较NC组增加了20.7%,P<0.01),并出现胰岛素抵抗(HOMA-IR:HF组为8.88±4.25,NC组为3.92±2.26熏P<0.05),空腹FFAs和TNF-α水平显著上升,较NC组分别增加了80.8%(P<0.05)和58.4%(P<0.05),但两组空腹血糖差异无显著性(HF组为7.89±1.46mmol/L,NC组为8.70±1.59mmol/L熏P>0.05)。结论高脂饮食可诱导大鼠肥胖伴胰岛素抵抗,其胰岛素抵抗的形成可能与TNFα、FFAs水平的升高有关。     

白藜芦醇对高脂饲养大鼠血液流变学的影响

摘要：目的：探讨白藜芦醇(Resveratrol)对高脂饲养大鼠血液流变学的影响。方法：将30只Wistar大鼠随机分为正常对照组(NC)、高脂组(HF)和白藜芦醇治疗组(Res)。16周后,检测各组大鼠血浆甘油三酯（TG）、总胆固醇（TC）和血液流变学指标。结果：与对照组相比,高脂组大鼠血浆TG和TC明显升高,全血粘度、血浆粘度、红细胞聚集指数、红细胞压积明显增大,红细胞变形指数减小;白藜芦醇能明显降低高脂大鼠血浆TG和TC水平(P<0.05),并且明显降低大鼠全血黏度(P<0.05)、血浆黏度(P<0.05)和红细胞聚集指数(P<0.05),提高红细胞变形指数(P<0.05)。结论：白藜芦醇改善高脂饲养大鼠的血液流变性可能与其降低血脂的功能有关。     

高脂饮食对大鼠胰岛素抵抗及氧化损伤指标的影响及意义

目的建立胰岛素抵抗(IK)大鼠模型并观察氧化应激指标的变化。方法将SD大鼠随机分为正常对照组(NC)及高脂饮食组(HFD),分别予普通饮食及高脂饮食6周,用高胰岛素正常血糖钳夹技术评价胰岛素敏感性;检测总抗氧化能力(TAOC)、超氧化物歧化酶(SOD)、丙二醛(MDA)等氧化应激指标,同时检测血总胆固醇(TC)、甘油三酯(TG)、游离脂肪酸(FFA)及胰岛素(Ins)水平。结果与NC组相比,HFD组的大鼠体重、血压、血糖、胰岛素水平明显高于NC组(P<0.05),而钳夹试验的结果显示IR组的葡萄糖输注率(GIR)低于NC组;HFD组出现明显的血脂代谢异常,TC、TG及FFA均高于NC组;HFD组MDA高于NC组,但TAOC和SOD却低于NC组。结论持续6周高脂饮食可成功复制胰岛素抵抗大鼠模型,IR状况下机体存在明显的氧化损伤。     

代谢综合征幼鼠血管VEGF和vWF的表达及意义

目的:探讨血管内皮生长因子(VEGF)和血管性假血友病因子(vWF)在代谢综合征(MS)幼鼠血管壁和血清中的表达及意义.方法:3周龄SD大鼠随机分为普通饮食组(NC组)、高脂组(FC组)和高脂+高盐组(FSC组).实验4周末测体质量、腹围、血压、内脏脂肪质量、血脂,行口服葡萄糖耐量试验,计算胰岛素抵抗指数.取腹主动脉免疫组化法检测血管壁VEGF和vWF表达,ELISA方法检测血清VEGF和vWF表达.结果:FSC组体质量、腹围、血压、内脏脂肪、血糖、胰岛素水平均较NC组增加,血脂紊乱加重,并出现胰岛素抵抗.FC组仅体质量、内脏脂肪质量高于NC 组,其他上述指标差异无统计学意义.FSC组血管壁及血清中VEGF和vWF较NC组和FC组均升高.FC组较NC组血管VEGF及血清中VEGF和vWF均升高.结论:VEGF和vWF参与了血管壁的功能紊乱或损伤的病生理改变.     

高脂高盐饮食对未成年鼠生长及代谢的影响

目的 观察高脂高盐饮食对未成年鼠生长发育、胰岛素敏感性及相关代谢指标的影响. 方法 40只体质量50g左右SD鼠（生长至3周末,刚断乳）随机分为三组：普通饮食组（NC组）12只、高脂组（FC组）14只、高脂高盐组（FSC组）14只,分别给予普通食物、高脂食物、高脂＋高盐食物喂养4周（鼠生长至7周末）,观察三组大鼠体质量、血压及内脏脂肪重量、血脂等,行口服葡萄糖耐量试验及胰岛素释放试验评价血糖及胰岛细胞功能. 结果 FSC组鼠体质量、内脏脂肪、血糖及胰岛素水平均较NC组明显增加,血脂紊乱加重并表现出显著的胰岛素抵抗,差异有统计学意义（均P＜0.05）. 结论 高脂高盐饮食可诱导未成年鼠腹型肥胖、高血压、血脂异常及糖耐量异常.     

High fat diet increases the incidence of orofacial dyskinesia and oxidative stress in specific brain regions of rats

Haloperidol-induced orofacial dyskinesia (OD) is a putative animal model of tardive dyskinesia (TD) whose pathophysiology has been related to free radical generation and oxidative stress. Schizophrenic patients have been reported to eat a diet higher in fat than the general population and dietary fat intake can lead to an increase in oxidative stress in animal models. The objective of this study was to determine whether association of ingestion of a high fat diet with prolonged haloperidol treatment could lead to OD and oxidative stress in the rat brain. Haloperidol decanoate administration (38 mg/kg, IM, which is equivalent to 1 mg/kg/day) monthly for a period of 6 months to rats fed previously with a high fat and normo fat diets (6 months) caused a increase in vacuous chewing (VCM) and duration of facial twitching (FT). Haloperidol caused a reduction in body weight gain and the loss of body weight occurred after 4 months of treatment with haloperidol. The effects on body weight were more accentuated in HF diet group. HF diet ingestion was associated with an increase in TBARS levels in cerebellum and cerebral cortex (regardless of haloperidol treatment). A significant dietxhaloperidol treatment interaction in striatum, subcortical parts and the region containing the substantia nigra was observed for TBARS. In fact, haloperidol caused an increase in TBARS levels of these regions only in rats fed with the HF. These results indicate that a high fat diet caused a transitory increase in haloperidol-induced OD in rats and this in part can be related to the haloperidol-induced oxidative stress in brain structures involved with OD.     

机械加载改善高脂饮食诱导的肥胖相关骨丢失

目的 探究脉冲式关节机械加载对高脂饮食诱导的肥胖小鼠骨丢失的改善作用。方法 将 45只雌性C57BL/6小鼠随机分为普通饮食对照组（Sham组）、高脂饮食模型组（HF组）和高脂加载治疗组（HF+L组）,每组 15只。HF组和 HF+L组高脂饮食喂养 4周后,HF+L组进行 4周的机械加载治疗（加载条件为 1 N,10 Hz,3 min/d,每周连续加载 5 d）。治疗结束后测量 3组小鼠体质量指数（BMI）、全身体脂含量和双侧股骨的骨密度。使用 HE染色和MacNeal’s染色分析观察股骨的组织病理改变,使用 Western blot检测成骨生成相关蛋白［碱性磷酸酶（ALP）、Runt相关转录因子 2（RUNX2）］和脂肪生成相关蛋白［过氧化物酶体增殖物激活受体 γ（PPARγ）、CCAAT/增强子结合蛋白 α（C/EBPα）］的表达。结果 与 Sham组相比,HF组小鼠的体脂含量和 BMI升高,骨密度变化率和骨量变化率显著下降,骨小梁面积明显减少,骨髓脂肪细胞增多。机械加载治疗后,HF+L组的骨密度、骨小梁面积比 HF组明显升高,脂肪细胞的数目和面积比 HF 组显著降低（P＜0.05）。Western blot 分析结果表明,HF+L 组与 HF 组相比,ALP 和RUNX2的表达显著升高,C/EBPα和 PPARγ的表达明显降低（均P＜0.05）。结论 机械加载能够有效缓解由肥胖引起的低骨密度和低骨量,其治疗作用可能通过促进成骨分化和抑制脂肪生成来改善骨丢失。     

胰岛素强化治疗对2型糖尿病大鼠氧化应激的影响研究

目的探讨胰岛素强化治疗对2型糖尿病(T2DM)大鼠氧化应激的影响,为临床胰岛素强化治疗提供理论依据。方法将36只Wistar大鼠随机分为正常对照组(NC组,n=12)和高脂组(HF组,n=24),将HF组大鼠造成T2DM模型后再随机分为2个亚组,即糖尿病对照组(DC组,n=12)和胰岛素治疗组(IT组,n=12)。IT组大鼠皮下注射胰岛素,NC组和DC组大鼠皮下注射等容积0.9%氯化钠溶液,疗程4周,比较3大鼠实验前后血清及肝组织中超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽转移酶(GSM)水平。结果 IT组血清及肝组织中SOD、GSM较DC组升高,差异有统计学意义(P<0.05);DC组较NC组降低,差异有统计学意义(P<0.01);IT组较NC组降低,差异有统计学意义(P<0.05)。IT组血清及肝组织中MDA较DC组降低,差异有统计学意义(P<0.05);DC组较NC升高,差异有统计学意义(P<0.01);IT组较NC组升高,差异有统计学意义(P<0.05)。结论 T2DM大鼠存在脂质过氧化水平升高及抗氧化酶活性下降,胰岛素强化治疗可减轻T2DM大鼠的氧化应激损伤,其机制与改善血脂代谢紊乱,减轻脂毒性有关。     

内质网应激对Nrf2抗氧化系统调控与高脂诱导的胰岛素抵抗发病机理研究

目的：探讨内质网应激对氧化还原平衡作用及其诱导胰岛素抵抗机制信号机理。方法随机将30只C57BL／6J小鼠分为低脂饲料对照组（LFD组,n＝10）和高脂饲料模型组（HFD组,n＝20）,14周后,经葡萄糖耐量试验（IPGTT）确定胰岛素抵抗模型成功后,HFD 组随机选出10只开始进行4-PBA药物干预（HFD＋PBA 组,n ＝10）,持续1周后检测小鼠葡萄糖耐量（IPGTT）、肌肉和肝脏及相应组织线粒体中丙二醛（ MDA）含量;Western blot检测肌肉和肝脏组织中胰岛素信号、内质网应激信号和Nrf2内源性抗氧化系统相关蛋白的表达。结果4-PBA干预组胰岛素抵抗明显减轻,PTEN蛋白受到抑制从而上调胰岛素信号（ PKB Ser473）;4-PBA干预组MDA水平明显下降,Nrf2系统信号增强;高脂组Keap1蛋白明显上调,而4-PBA干预则减弱这一变化。结论内质网应激造成氧化应激并通过上调 PTEN蛋白和抑制 Nrf2抗氧化系统参与胰岛素抵抗。     

Metabolic disorders and oxidative stress programming in offspring of rats fed a high-fat diet during lactation: effects of a vinifera grape skin (ACH09) extract

This study examined the effect of Vitis vinifera grape skin ACH09 extract (ACH09) on metabolic disorders and oxidative stress in adult offspring of rats fed a high-fat diet (HF) during lactation. Four groups of female rats were fed: control diet (7% fat); ACH09 (7% fat + 200 mg·kg·d ACH09 orally); HF (24% fat); HF+ ACH09 (24% fat + 200 mg·kg·d ACH09 orally) during lactation. From weaning onward, all female offspring were fed a control diet and killed when they were 90 or 180 days old. Systolic blood pressure was increased in adult offspring of HF-fed dams, and ACH09 prevented hypertension. Increased adiposity, plasma triglyceride, glucose levels, and insulin resistance were observed in offspring from both ages, and these changes were reversed by ACH09. The plasma oxidative damage assessed by malondialdehyde levels was increased, and nitrite levels decreased in the HF group of both ages, which were reversed by ACH09. In addition, ACH09 restored the decreased plasma and mesenteric artery antioxidant activities of superoxide dismutase, catalase, and glutathione peroxidase in the HF group. In conclusion, ACH09 protected normally fed offspring of HF-fed dams during lactation from phenotypic and metabolic characteristics of metabolic syndrome providing an alternative nutritional resource for the prevention of metabolic syndrome.     

Similar changes in muscle lipid metabolism are induced by chronic high‐fructose feeding and high‐fat feeding in C57BL/J6 mice

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Therapy with resveratrol attenuates obesity-associated allergic airway inflammation in mice

Obesity and insulin resistance have been associated with deterioration in asthma outcomes. High oxidative stress and deficient activation of AMP-activated protein kinase (AMPK) have emerged as important regulators linking insulin resistance and inflammation. This study aimed to evaluate the effects of resveratrol on obesity-associated allergic pulmonary inflammation. Male C57/Bl6 mice fed with high-fat diet to induce obesity (obese group) or standard-chow diet (lean group) were treated or not with resveratrol (100 mg/kg/day, two weeks). Mice were sensitized and challenged with ovalbumin (OVA). At 48 h thereafter, bronchoalveolar lavage fluid was performed, and lungs collected for morphological studies and Western blot analysis. Treatment of obese mice with resveratrol significantly reduced hyperglycemia and insulin resistance, as well as the body measures (body mass, fat mass, % fat, and body area). OVA-challenge promoted a higher increase in pulmonary eosinophil infiltration in obese compared with lean mice, which was nearly abrogated by resveratrol treatment. Resveratrol markedly increased the phosphorylated AMPK expression in lung tissues of obese compared with lean mice. Resveratrol reduced the p47phox expression and reactive-oxygen species (ROS) production, and elevated the superoxide dismutase (SOD) levels in lung tissues of obese mice. The increased pulmonary levels of TNF-α and inducible nitric oxide synthase (iNOS) in obese mice were also normalized after resveratrol treatment. In lean mice, resveratrol failed to affect the levels of fasting glucose, p47phox, ROS levels, TNF-α, iNOS and phosphorylated AMPK. Resveratrol exhibits protective effects in obesity-associated lung inflammation that is accompanied by local AMPK activation and antioxidant property.     

白藜芦醇改善高脂喂养大鼠胰岛素抵抗的机制

目的:观察白藜芦醇(Res)对高脂喂养大鼠胰岛素抵抗的影响并初步探讨其机制。方法:将30只♂Wistar大鼠随机分为对照组(NC组)及高脂组(HF组),分别给予基础饲料和高脂饲料喂养;喂养6周后,对HF组大鼠进行胰岛素敏感性造模,再将造模成功的大鼠随机分为模型组(IR组)和Res干预组(RT组),继续给予高脂饲料喂养,RT组同时给予100 mg.kg-1.d-1Res灌胃,共持续10周。第16周末,处死各组大鼠,测量各组大鼠的体质量及肾周和附睾脂肪,脂肪组织石蜡切片HE染色观察脂肪细胞大小,并应用ELISA检测血清脂联素(APN)的水平。结果:第16周后I,R组大鼠与NC组相比,表现出内脏型肥胖,肾周脂肪细胞的面积明显增加,胰岛素敏感性及血清APN水平均显著下降;Res的干预可减轻RT组大鼠内脏型肥胖,降低肾周脂肪细胞的面积,改善胰岛素抵抗,并且明显上调血清APN水平;与NC组比较,RT组大鼠脂肪细胞面积仍然显著大于NC组;胰岛素敏感性及血清APN水平仍然显著低于NC组。结论:Res的干预可以改善高脂喂养大鼠的胰岛素抵抗;其机制可能与其在改善高脂喂养大鼠的内脏型肥胖的同时升高血清APN水平有关。     

肥胖大鼠非酒精性脂肪肝与血清脂联素和肿瘤坏死因子α的关系及吡格列酮干预

目的观察营养性肥胖大鼠非酒精性脂肪肝(NAFLD)与血清脂联素和肿瘤坏死因子α(TNF-α)的关系,以及吡格列酮干预后的变化。方法45只SD♂大鼠随机分为3组:吡格列酮组(P)、高脂对照组(HF)和普通饮食组(NC),各15只。P、HF组给予高脂饮食,NC组给予普通饲料;12wk后,P组行吡格列酮10mg·kg-1.d-1灌胃,HF组和NC组用相应溶剂灌胃,均灌胃4wk。检测血清脂联素、TNF-α、游离脂肪酸(FFA)水平和其他生化指标等,计算Lee′s指数、HOMA-IR指数和肝脏指数,行肝脏病理切片和HE染色。结果与NC组相比,HF组大鼠体重、肝脏指数、FPG、FINS、ALT、HOMA-IR和血清TNF-α水平均明显增高,血清脂联素水平降低(P<0.05),肝细胞出现脂肪变性。与HF组比较,P组大鼠肝脏指数、HOMA-IR、FFA、TNF-α均降低,脂联素水平升高(P<0.05),肝细胞脂肪变性明显改善。HF组大鼠血清FFA、TNF-α与HOMA-IR、肝脏指数正相关,脂联素与之负相关(P<0.05)。结论高脂饮食可引起大鼠营养性肥胖、胰岛素抵抗和NAFLD;吡格列酮能提高胰岛素敏感性,改善脂肪细胞变性,可能与降低TNF-α、升高脂联素有关。     

代谢综合征未成年鼠肝脏5α-R1表达及其对肾上腺皮质功能的调控

[摘要]目的:探讨代谢综合征未成年鼠肝脏中皮质醇代谢关键酶5α-还原酶1表达及其对肾上腺皮质功能的影响。方法: 方法:50克左右雄、雌性SD大鼠随机分为3组:普通饮食组(NC组);高脂组(FC组);高脂十高盐组(FSC组)。实验四周末测体重、体长、腹围、血压,观测内脏脂肪重量、血脂、血皮质醇、促肾上腺皮质激素释放激素等,行口服葡萄糖耐量试验及胰岛素释放试验。取肾上腺称重,取新鲜肝组织,测5α-还原酶1mRNA表达水平。结果: 高脂高盐饮食使未成年鼠体重、腹围、血压、内脏脂肪、血糖、胰岛素水平均比普通饮食组显著增加,血脂紊乱加重并表现出显著的胰岛素抵抗。该组肝脏5α-还原酶1 mRNA增加,并与肾上腺重量、血皮质醇及促肾上腺皮质激素释放激素水平显著相关。 结论: 我们成功以高脂高盐饮食诱导了代谢综合征未成年鼠模型,肝脏组织高表达5α-还原酶1可正性调控肾上腺皮质功能。提示针适时适当干预5α-还原酶1表达和活性可能是代谢综合征干预策略之一。     

Anti‐contractile effects of perivascular adipose tissue in thoracic aorta from rats fed a high‐fat diet: role of aerobic exercise training

The aim of the present study was to evaluate the effects of aerobic exercise training on perivascular adipose tissue (PVAT) function in thoracic aorta from rats fed a high‐fat diet. Aortic vascular reactivity was performed in sedentary (SD), trained (TR), sedentary high‐fat diet (SD‐HF), and trained high‐fat diet (TR‐HF) male Wistar rats in the absence (PVAT?) or in the presence (PVAT+) of thoracic PVAT. We also measured circulatory concentrations of leptin and tumour necrosis factor alpha (TNF‐α), as well as the protein expressions of TNF‐α receptor 1 (TNFR1) and inducible nitric oxide synthase (iNOS) on PVAT. In the SD‐HF group, the body weight, epididymal fat pad, thoracic PVAT, circulatory triglycerides, insulin, leptin and TNF‐α were increased when compared with the SD group, whereas exercise training reduced these values in TR‐HF group. The relaxing response curves to acetylcholine and sodium nitroprusside were not modified by either intervention (high‐fat diet or exercise training) or the presence of PVAT. The presence of PVAT had an anti‐contractile effect in response to serotonin in all groups. In SD‐HF group, the increased magnitude of anti‐contractile effects was in parallel with an up‐regulation of iNOS protein expression in PVAT without alteration in TNFR1. Exercise training was effective in normalizing the vascular reactivity in rings PVAT+ and in reducing the iNOS protein expression. Exercise training prevented the PVAT–induced alteration in thoracic aorta from rats fed a high‐fat diet.