红霉素对糖尿病结肠运动障碍干预作用及其影响因素分析

目的　应用红霉素对糖尿病 (DM)大鼠离体近端结肠平滑肌自发性收缩的干预 ,探讨其对糖尿病结肠运动障碍的作用、以及与结肠平滑肌运动、血浆和结肠组织中生长抑素 (SS) ,血管活性肠肽 (VIP) ,胃动素 (MTL) ,P物质 (SP)等的相互关系。方法　建立DM大鼠模型 :DM组 (n =10 )、DM红霉素治疗组 (n =10 )和对照组 (n =10 ) ;制备三组大鼠离体近端结肠环行肌及纵行肌肌条 ,应用张力换能器测定肌条自发性等长收缩时的静息张力、平均振幅、收缩频率等运动指标 ;同时各组大鼠分别采血和取近端结肠组织 ,用放免法同批测定三组大鼠血浆和结肠组…     

高脂饮食诱发血糖升高的动物模型中瘦素与胰岛素变化的关系

高脂饲料喂养大鼠,诱发胰岛素抵抗形成血糖升高,以研究瘦素与糖尿病的关系。将大鼠分为正常和高脂饲料喂养组,于喂养前及喂养30、60d时测血糖、瘦素与胰岛素水平,行高胰岛素正常血糖钳夹试验,最后分离分离脂肪称重。结果：高脂饮食组具有明显的胰岛素抵抗,有50％血糖升至8．3mmol/L以上;形成糖尿病的大鼠体重与对照组无明显区别;高脂饮食组瘦素与胰岛素水平与对照组比较有明显差异;所有大鼠瘦素水平与体重、胰岛素、血糖均呈正相关。结论：（1）高脂饮食是导致胰岛素抵抗形成糖尿病的诱因之一;（2）体脂含量与糖尿病正相关;（3）瘦素抵抗与胰岛素抵抗形成糖尿病的发病机制可能有关;（4）瘦素水平随着鼠龄的增加而增高,且参与体重的调节。     

2.67红霉素对糖尿病结肠运动障碍干预作用及其影响因素分析

目的应用红霉素对糖尿病(DM)大鼠离体近端结肠平滑肌自发性收缩的干预,探讨其对糖尿病结肠运动障碍的作用、以及与结肠平滑肌运动、血浆和结肠组织中生长抑素(SS),血管活性肠肽(VIP),胃动素(MTL),P物质(SP)等的相互关系.     

AMPK/PGC-1α在有氧运动改善2型糖尿病大鼠骨骼肌萎缩中的作用

文题释义：腺苷酸活化蛋白激酶(AMPK)：是生物能量代谢调节的关键分子,AMPK在低氧、缺血、运动和营养缺乏等条件下易被激活,是研究糖尿病及其他代谢相关疾病的核心因子。 肌萎缩：宏观上表现为肌肉体积和质量的降低,微观上表现为肌纤维数目或直径减少。骨骼肌是摄取和利用葡萄糖的重要组织,肌萎缩的发生将增加2型糖尿病等代谢性疾病的发病风险。 背景：腺苷酸活化蛋白激酶(AMP-activated kinase,AMPK)对线粒体能量代谢功能的调节障碍是导致肥胖和2型糖尿病患者脂肪堆积的重要原因,长期慢性炎症反应还将进一步诱导骨骼肌萎缩的发生,有氧运动可以提高AMPK的活性并调节能量代谢,但是通过有氧运动提高AMPK改善2型糖尿病骨骼肌萎缩的作用机制尚不明确。 目的：探究有氧运动对2型糖尿病大鼠骨骼肌萎缩的影响,以及AMPK在其中的作用机制。 方法：采用高脂饲养联合链脲佐菌素注射建立2型糖尿病大鼠模型20只,建模后将大鼠分为糖尿病组(n=8)和糖尿病运动组(n=12),同时将正常大鼠15只分为安静对照组(n=6)和运动组(n=9),其中安静对照组和糖尿病组继续饲养4周,运动组和糖尿病运动组进行有4周有氧运动干预(跑速16 m/min,60 min/d,5 d/周),运动干预后取大鼠比目鱼肌免疫组织化学染色观察各组肌萎缩情况,Western blot检测AMPK、PGC-1α、MAFbx和MuRF1蛋白表达情况。实验已于2016-06-25通过北京体育大学运动科学实验伦理委员会批准(批准号：2016014)。 结果与结论：①高脂饲养联合链脲佐菌素注射建立的2型糖尿病模型大鼠血糖显著升高、体质量和胰岛素水平显著下降(P < 0.01);②糖尿病组大鼠比目鱼肌肌纤维平均横截面积较安静对照组显著降低(P < 0.01),糖尿病运动组大鼠比目鱼肌肌纤维平均横截面积较糖尿病组显著升高(P < 0.01);③糖尿病组大鼠比目鱼肌中AMPK和PGC-1α表达水平较安静对照组显著降低,MAFbx和MuRF1表达水平较安静对照组显著升高(P < 0.01);糖尿病运动组大鼠AMPK表达水平较糖尿病组显著升高,MAFbx和MuRF1的水平较糖尿病组显著降低(P < 0.01);④上述结果说明,有氧运动通过激活AMPK/PGC-1α信号通路,提高线粒体功能,抑制MAFbx和MuRF1表达水平,改善骨骼肌萎缩,在一定程度上恢复了2型糖尿病的代谢平衡。 ORCID: 0000-0003-0979-7741(王继) 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

饮食模式对大鼠糖尿病早期肾脏病变的影响及其机制

目的：使用不同饮食模式联合链脲佐菌素（STZ）诱导建立大鼠糖尿病模型，确认模型结果并探索饮食模式对大鼠糖尿病早期肾脏病变的影响及其可能的机制。方法：将147只SD大鼠分别以正常饮食（维持饲料且自由摄食，n=25）、控制饮食（维持饲料但减量20%,n=25）和高脂饮食（高脂饲料且自由摄食，n=97）分组喂养后注射低剂量STZ，以空腹血糖是否达到糖尿病造模标准再分为未成模大鼠和成模大鼠，追踪动物的摄食、饮水和体重，通过组织病理学分析各组大鼠肾脏病变，采集各阶段的血浆样品并检测内源性代谢产物进而开展代谢组学分析。结果：不同饮食模式联合低剂量STZ可不同程度诱发大鼠糖尿病早期肾脏病变，主要表现为肾小管空泡变性，累及部分近曲小管和远曲小管。高脂饮食组的糖尿病成模率（89.2%）和肾脏病变率均最高（造模前期7/10，造模后期57/59），控制饮食组肾脏病变率最低（造模前期0/12，造模后期3/13）。相比正常饮食组，控制饮食组能量代谢和糖异生作用有关的代谢产物[如L-肉毒碱，不饱和脂肪酸二十四碳四烯酸（24:4n-6），氨基酸及其衍生物L-胱硫醚、4-氯-L-苏氨酸、L-酪氨酸等]有显著差异（P&...     

μ阿片受体在大鼠结肠肠肌丛的神经化学特性

目的:探索μ阿片受体(MOR)在大鼠结肠肠肌丛的分布及化学神经解剖学特性。方法:取大鼠结肠右曲和左曲之间肠管行全层铺片,剥离粘膜层、粘膜下层和环形肌层,保留纵行肌层。运用免疫荧光组织化学双重标记技术染色,共聚焦显微镜下观察MOR在大鼠结肠肠肌丛的分布及与一氧化氮合酶(NOS)、肠血管活血肽(VIP)、P物质(SP)或降钙素基因相关蛋白(CGRP)等在肠神经细胞的共存关系。结果:免疫荧光组织化学染色显示:在大鼠结肠肠肌层,MOR阳性细胞聚集形成神经节,其阳性突起穿行于神经节之间形成网格状神经丛。在肠肌丛神经细胞内,可见MOR分别与NOS、VIP、SP、CGRP共存。MOR阳性神经纤维和终末分布于NOS阳性神经细胞周围,也可见部分NOS、VIP阳性神经纤维和终末分布于MOR阳性神经细胞表面。有大量SP和CGRP阳性神经纤维穿行于MOR阳性神经细胞之间并包绕于MOR阳性神经细胞的胞体周围。结论:在结肠的肠肌丛,MOR与抑制性和感觉性神经递质在肠神经细胞有共存,且相互之间有纤维联系,推测MOR可能介导了阿片类调节肠神经细胞内抑制性神经递质的释放,并可能对肠感觉信息的传递有调节作用。     

低脂饮食和有氧运动干预对高脂大鼠脂肪组织蛋白激酶B表达的影响

目的 :观察低脂饮食和有氧运动对高脂大鼠脂肪组织中蛋白激酶B(PKB)表达的影响。方法 :选取雄性Wistar大鼠 4 0只 ,随机分为正常对照组 ( 10只 )和模型组 ( 30只 )。模型组大鼠给予高脂喂养 ,4周后 ,再随机分为 3组 :胰岛素抵抗组 ,继续高脂饮食 ;低脂饮食组 ,给予低脂饮食 ;有氧运动组 ,继续高脂饮食 +有氧运动。干预 6周后 ,蛋白印迹法检测大鼠脂肪组织中胰岛素刺激PKB表达的含量变化。结果 :低脂饮食组和有氧运动组大鼠空腹血糖 (FBG)、甘油三酯 (TG)、胆固醇 (TC)、内脏脂肪及胰岛素抵抗指数 (HOMA IR)下降 ,胰岛素敏感指数 (ISI)显著升高。而PKB蛋白表达分别增加了 16 .1%和 19.2 %(P <0 .0 1)。结论 :低脂饮食和有氧运动能改善胰岛素抵抗 ,可能与增加脂肪组织中PKB蛋白表达有关。     

P物质、血管活性肠肽和乙酰胆碱能神经在大鼠肠道内的分布及其关系

应用乙酰胆碱酯酶(AChE)组织化学和PAP免疫组织化学方法,比较观察P物质(SP)、血管活性肠肽(VIP)和AChE三种阳性神经元在大鼠十二指肠、空肠、回肠、结肠和直肠内的分布特征及其相互关系。结果显示:SP、VIP、AChE阳性神经神经元和纤维均分布于肠壁各层,从十二指肠、空肠到回肠逐渐增多,但从结肠到直肠则逐渐减少;AChE阳性神经元或纤维在肠壁各层最丰富,其中VIP以粘膜层和粘膜下神经丛较丰富,SP以肠肌丛较丰富;三者的分布密度为AChE>VIP>SP。AChE、SP和VIP阳性神经元胞体及神经纤维在不同肠段的分布密度有明显差异(P<0.05),提示可能与不同肠段肠动力调节功能有关。     

有氧和抗阻运动可缓解2型糖尿病模型大鼠的肝脏炎症反应

背景:2型糖尿病可诱发肝脏炎症,运动已被证明可改善糖尿病,但机制尚不清楚.目的:探讨有氧及抗阻运动对2型糖尿病大鼠肝脏炎症状态的影响.方法:SD雄性大鼠随机分为6组,分别为空白对照组、有氧运动组、抗阻运动组、糖尿病模型组、糖尿病有氧运动组、糖尿病抗阻运动组,每组8只.高糖高脂联合小剂量链脲佐菌素构建2型糖尿病动物模型;...     

不同强度电针对肥胖大鼠附睾脂肪细胞内质网应激的影响

 目的:通过观察SD肥胖大鼠附睾脂肪组织中脂肪细胞内质网应激-未/折叠蛋白反应（unfolded protein response,UPR）信号转导通路中信号分子p-PERK、CHOP/GADD153、 Bcl-2及caspase-12的含量,探索电针对内质网应激的影响。方法:将60只SD大鼠随机分为普食组(n=10)和高脂饮食组（n=50）,分别以普通饮食及高脂饮食喂养。10周后选取30只超过普食组大鼠体重20%的高脂饮食组肥胖大鼠进行电针治疗,数字随机分组：高脂饮食组（n=10）、5 mA电针组（n=10）和1 mA电针组（n=10）。高脂饮食组不针刺,电针组针刺双侧足三里（ST 36）和三阴交（SP 6）,电针参数选择：疏密波,频率20 Hz,强刺激电针组选用5 mA,弱刺激电针组选用1 mA。2周后治疗结束。用Western blotting检测肥胖大鼠附睾脂肪组织p-PERK和CHOP/GADD153的表达,酶联免疫吸附法（ELISA）检测细胞凋亡相关的Bcl-2及caspase-12的含量。结果:体重：高脂饮食组较普食组增加34.99%,5 mA电针组较普食组增加7.55%,1 mA电针组较普食组增加15.50%（P<0.01或P<0.05）;Bcl-2的含量：高脂饮食组较普食组增加20.45%,5mA电针组较普食组增加4.93%,1 mA电针组较普食组增加6.57%,（P<0.01）;caspase-12的含量：高脂饮食组较普食组增加53.64%,5 mA电针组较普食组增加7.49%,1 mA电针组较普食组增加24.51%,（P<0.01）;p-PERK表达：高脂饮食组较普食组增加251.61%,5 mA电针组较普食组增加61.29%,1 mA电针组较普食组增加145.16%（P<0.01）;CHOP/GADD153表达：高脂饮食组较普食组增加438.46%,5 mA电针组较普食组增加26.32%,1 mA电针组较普食组增加184.21%（P<0.01）。结论: 电针“足三里”和“三阴交”穴能降低p-PERK、CHOP/GADD153、 Bcl-2和caspase-12的含量,5 mA电针组比1 mA电针组效果好。电针能抑制肥胖时机体脂肪细胞的内质网应激反应,本实验结果为电针治疗肥胖炎症状态提供依据。     

The effects of different types of aquatic exercise training interventions on a high-fructose diet-fed mice

Gradual weight gain in modern people and a lowering onset age of metabolic disease are highly correlated with the intake of sugary drinks and sweets. Long-term excessive fructose consumption can lead to hyperglycemia, hyperlipidemia and accumulation of visceral fat. Abdominal obesity is more severe in females than in males. In this study, we used a high-fructose-diet-induced model of obesity in female mice. We investigated the effects of aquatic exercise training on body weight and body composition. After 1 week of acclimatization, female ICR mice were randomly divided into two groups: a normal group (n=8) fed standard diet (control), and a high-fructose diet (HFD) group (n=24) fed a HFD. After 4 weeks of induction followed by 4 weeks of aquatic exercise training, the 24 obese mice were divided into 3 groups (n=8 per group): HFD with sedentary control (HFD), HFD with aquatic strength exercise training (HFD+SE), and HFD with aquatic aerobic exercise training (HFD+AE). We conducted serum biochemical profile analysis, weighed the white adipose tissue, and performed organ histopathology. After 4 weeks of induction and 4 weeks of aquatic exercise training, there was no significant difference in body weight among the HFD, HFD+SE and HFD+AE groups. Serum triglyceride (TG), AST, ALT, and uric acid level were significantly lower in the HFD+SE and HFD+AE groups than in the HFD group. The weight of the perirenal fat pad was significantly lower in the HFD+AE group than in the HFD group. Hepatic TG and total cholesterol (TC) were significantly lower in the HFD+AE group than in the other groups. Long-term intake of a high-fructose diet can lead to obesity and increase the risk of metabolic disease. Based on our findings, we speculate that aquatic exercise training can effectively promote health and fitness. However, aquatic aerobic exercise training appears to have greater benefits than aquatic strength exercise training.     

Isolated obesity resistance condition or associated with aerobic exercise training does not promote cardiac impairment

Mechanisms involved in cardiac function and calcium (Ca²⁺) handling in obese-resistant (OR) rats are still poorly determined. We tested the hypothesis that unsaturated high-fat diet (HFD) promotes myocardial dysfunction in OR rats, which it is related to Ca²⁺ handling. In addition, we questioned whether exercise training (ET) becomes a therapeutic strategy. Male Wistar rats (n=80) were randomized to standard or HFD diets for 20 weeks. The rats were redistributed for the absence or presence of ET and OR: control (C; n=12), control + ET (CET; n=14), obese-resistant (OR; n=9), and obese-resistant + ET (ORET; n=10). Trained rats were subjected to aerobic training protocol with progressive intensity (55-70% of the maximum running speed) and duration (15 to 60 min/day) for 12 weeks. Nutritional, metabolic, and cardiovascular parameters were determined. Cardiac function and Ca²⁺ handling tests were performed in isolated left ventricle (LV) papillary muscle. OR rats showed cardiac atrophy with reduced collagen levels, but there was myocardial dysfunction. ET was efficient in improving most parameters of body composition. However, the mechanical properties and Ca²⁺ handling from isolated papillary muscle were similar among groups. Aerobic ET does not promote morphological and cardiac functional adaptation under the condition of OR.     

吡咯烷二硫代氨基甲酸酯对2型糖尿病大鼠心肌的保护作用

目的: 探讨吡咯烷二硫代氨基甲酸酯(PDTC)的降糖作用及对糖尿病大鼠心肌的保护作用。方法: 37只雄性Wistar大鼠,随机分为正常对照组(NC)和高脂饮食组(HFD)。喂养8周后,高脂饮食组大鼠腹腔注射单剂量链脲佐菌素(STZ)27 mg/kg复制2型糖尿病大鼠模型。造模成功后再随机分为模型组和PDTC治疗组。PDTC治疗组大鼠每天腹腔注射PDTC(50 mg/kg)1次,模型组和正常对照组每天注射相同剂量的生理盐水,连续注射1周后,检测血糖及各种生化指标,处死大鼠。检测心肌组织中丙二醛(MDA)含量、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)的活性;用透射电镜观察心肌组织的超微结构;用免疫组化观察心肌组织中诱导型一氧化氮合酶(iNOS)和硝基酪氨酸(NT)的表达。结果: 糖尿病模型组与正常对照组大鼠相比,血糖和MDA水平显著升高,SOD和GSH-Px活性明显下降(P<0.01);PDTC治疗后,血糖和MDA水平明显降低,SOD和GSH-Px活性明显升高(P＜0.01)。糖尿病组心肌变性坏死、线粒体损伤及炎症细胞浸润;PDTC治疗后线粒体损伤明显减轻。糖尿病组较正常对照组心肌中iNOS和NT的表达均明显增加;PDTC治疗后iNOS和NT的表达均明显减少。结论: 高血糖可引起氧化应激,使心肌组织中iNOS和NT生成过多,损伤了心肌细胞的结构和功能。PDTC不仅具有降糖作用,而且还可以通过减少iNOS和NT的产生,进而阻止或延缓糖尿病心肌病的发生。     

Effect of Regular Exercise on the Histochemical Changes of d-Galactose-Induced Oxidative Renal Injury in High-Fat Diet-Fed Rats

Renal lipid accumulation exhibits slowly developing chronic kidney disease and is associated with increased oxidative stress. The impact of exercise on the obese- and oxidative stress-related renal disease is not well understood. The purpose of this study was to investigate whether a high-fat diet (HFD) would accelerate d-galactose-induced aging process in rat kidney and to examine the preventive effect of regular exercise on the obese- and oxidative stress-related renal disease. Oxidative stress was induced by an administration of d-galactose (100 mg/kg intraperitoneally injected) for 9 weeks, and d-galactose-treated rats were also fed with a high-fat diet (60% kcal as fat) for 9 weeks to induce obesity. We investigated the efficacy of regular exercise in reducing renal injury by analyzing Nε-carboxymethyllysine (CML), 8-hydroxygluanine (8-OHdG) and apoptosis. When rats were fed with a HFD for 9 weeks in d-galactose-treated rats, an increased CML accumulation, oxidative DNA damage and renal podocyte loss were observed in renal glomerular cells and tubular epithelial cells. However, the regular exercise restored all these renal changes in HFD plus d-galactose-treated rats. Our data suggested that long-term HFD may accelerate the deposition of lipoxidation adducts and oxidative renal injury in d-galactose-treated rats. The regular exercise protects against obese- and oxidative stress-related renal injury by inhibiting this lipoxidation burden.     

高脂饮食对大鼠海马、大脑皮质和脊髓GDNF表达的影响

目的:探讨高脂饮食对大鼠海马、大脑皮质和脊髓胶质细胞源性神经营养因子(GDNF)的影响。方法:20只雄性SD大鼠随机分成两组:普通饮食组(ND)和高脂饮食组(HFD),每组10只,分别给子两组大鼠普通饮食和高脂饮食14周,测量各组大鼠体重脂肪重、Lee's指数和脂体比。应用real time RT-PCR检测各组大鼠海马、大脑皮质和脊髓GDNFmRNA的表达;应用Western Blot检测各组大鼠海马、大脑皮质和脊髓CDNF蛋白的表达;应用酶联免疫吸附实验(ELISA)检测各组大鼠海马、大脑皮质和脊髓肿瘤坏死因子-α(TNF-α)、白细胞介索-1β(IL-1β)和IL-6的水平。结果:高脂饮食导致大鼠体重、脂肪重,Lee's指数和脂体比均明显升高(P<0.05);HFD组大鼠海马、大脑皮质和脊髓GDNF mRNA表达水平较ND组均显著下降(P<0.01),HFD组大鼠海马、大脑皮质和脊髓GDNF蛋白表达水平较ND组均明显下降(P<0.05);HFD组大鼠海马、大脑皮质和脊髓中TNF-α、IL-1β和IL-6水平与ND组相比均明显升高(P<0.01)。结论:高脂饮食造成大鼠肥胖,降低了大鼠海马、大脑皮质和脊髓GDNF的表达水平,同时促进了炎症反应的发生。     

Distribution and chemical coding of intramural neurons in the porcine ileum during proliferative enteropathy

Enteric neurons are highly adaptive in their response to various pathological processes including inflammation, so the aim of this study was to describe the chemical coding of neurons in the ileal intramural ganglia in porcine proliferative enteropathy (PPE). Accordingly, juvenile Large White Polish pigs with clinically diagnosed Lawsonia intracellularis infection (PPE; n=3) and a group of uninfected controls (C; n=3) were studied. Ileal tissue from each animal was processed for dual-labelling immunofluorescence using antiserum specific for protein gene product 9.5 (PGP 9.5) in combination with antiserum to one of: vasoactive intestinal polypeptide (VIP), substance P (SP), calcitonin gene-related peptide (CGRP), somatostatin (SOM), neuropeptide Y (NPY) or galanin (GAL). In infected pigs, enteric neurons were found in ganglia located within three intramural plexuses: inner submucosal (ISP), outer submucosal (OSP) and myenteric (MP). Immunofluorescence labelling revealed increases in the number of neurons containing GAL, SOM, VIP and CGRP in pigs with PPE. Neuropeptides may therefore have an important role in the function of porcine enteric local nerve circuits under pathological conditions, when the nervous system is stressed, challenged or afflicted by disease such as PPE. However, further studies are required to determine the exact physiological relevance of the observed adaptive changes.     

Intestinal mucosal barrier dysfunction participates in the progress of nonalcoholic fatty liver disease

Intestinal mucosal barrier dysfunction is closely related to liver diseases, which implies impaired gut-liver axis may play a role in the pathogenesis of NAFLD. In our study, rats were divided into three groups: normal chow diet (NCD) group, high-fat diet (HFD) group and TNBS-induced colitis with high-fat diet (C-HFD) group. Liver tissues were obtained for histological observation and TNF-α, IL-6 mRNA determination and blood samples were collected for liver enzymes and LPS analysis. Ultrastructural changes of jejuna epithelium, SIBO and amounts of CD103⁺MHCII⁺DCs and CD4⁺CD25⁺FoxP3⁺T-regs in terms of percentage in mesenteric lymph nodes (MLN) were observed by electron microscope, bacterial cultivation and flow cytometry, respectively. The results demonstrated the pathological characteristics accorded with nonalcoholic simple fatty liver (NAFL) and NASH in HFD group by week 8 and 12, respectively. Besides, the degree of hepatic steatosis and steatohepatitis was more severe in C-HFD group compared with HFD-group at the same time point. NAFLD activity score (NAS), liver enzymes, concentration of LPS and mRNA expressions of TNF-α, IL-6 were higher significantly in C-HFD group compared with HFD and NCD group at week 4, 8 and 12, respectively. In HFD group, epithelium microvilli atrophy, disruptive tight junctions and SIBO were present, and these changes were more severe in NASH compared with NAFL. The percentage of CD103+MHCII+DCs and CD4+CD25+FoxP3+T-regs decreased significantly in NAFL and NASH compared with NCD group. Our conclusion was that gut-liver axis was impaired in NAFLD, which played crucial role in the pathogenesis of NAFLD.     

高脂膳食和跑台运动构建模型大鼠腓肠肌葡萄糖转运体4和cAMP反应元件结合蛋白的变化

BACKGROUND: Some studies indicate that PI3K/Akt signaling pathway is associated with the expression of glucose transporter 4 (GLUT4) and the function of cAMP response element binding protein (CREB) in skeletal muscle. However, it is still unclear whether PI3K/Akt signaling pathway has the effects on CREB and GLUT4 in skeletal muscle of the rats with high-fat diet and treadmill exercise. OBJECTIVE: To investigate whether PI3K/Akt signaling pathway has the effects on CREB and GLUT4 in gastrocnemius muscle of the rats with high-fat diet and treadmill exercise.  METHODS: A total of 70 rats were fed with normal diet for 2 weeks, and randomly divided into common feed group (n=20) and high-fat feed group (n=50). Rats in both groups were respectively fed with common feed and high-fat feed for 8 weeks. The rats in the common feed group were equally assigned to common feed quiet group and common feed exercise group. 20 rats from the high-fat feed group whose body weight was 1.4 times of common rats were randomly and equally assigned to obese quiet group and obese exercise group. Rats in the quiet groups did not do exercises. Rats in the exercise groups received adaptive sports for 1 week and medium-intensity treadmill exercise for 8 weeks.  RESULTS AND CONCLUSION: (1) Impairments of PI3K/Akt signaling pathway appeared in obese rats, however, the quantity of GLUT4 expression did not change obviously in gastrocnemius muscles of obese rats. The reasons for the decrease of the nuclear protein CREB level of gastrocnemius muscles of obese rats might be related to the decrease of pAkt-Ser473 level. (2) The increase of the quantity of GLUT4 expression was accompanied by significantly up-regulated pAkt-Ser473 level by exercise intervention in gastrocnemius muscles of obese rats. Exercise intervention significantly increased the expression of nuclear protein CREB in gastrocnemius muscles of chow-fed rats and obese rats, which was consistent with the changes of pAkt-Ser473. These findings suggest that pAkt-Ser473 can play an important role in the effects of high-fat diet and exercise intervention on GLUT4 and CREB protein expression in gastrocnemius muscles of obese rats.       

Effect of the detraining status on high-fat diet induced fat accumulation in the adipose tissue and liver in female rats

The purpose of the present study was to investigate the effects of a high-fat diet (HFD) in previously trained rats that have been detrained for different periods. Two groups of female rats were, first, either treadmill trained for 8 weeks or remained sedentary (Sed). Trained animals, thereafter, remained inactive for 4 weeks (Inact-4 weeks), while fed a standard diet, before being submitted to a high-fat diet (42% kcal of fat) for an additional 2 or 6 weeks. The order was reversed in a 3rd group in which rats were first kept sedentary for 4 weeks before being submitted to the same 8-week training program that ended with the initiation of the HFD (Inact-0 week). Fat accumulation in the mesenteric depot (P<0.05) and in the sum of 3 intra-abdominal (urogenital, retroperitoneal, and mesenteric; P=0.065) tissues in response to the HF feeding was higher in trained rats kept inactive for 4 weeks than in Sed and Inact-0 week animals. Liver triacylglycerol accumulation also showed a tendency to be higher (P<0.07) in Inact-4 weeks than in Inact-0 week rats. These changes were not associated with significant changes in fat cell diameter and number in the mesenteric adipose tissue. When rats in all groups were subdivided into obesity prone (OP) and obesity resistant (OR) on the basis of the change in body weight gain in response to the HFD, liver lipid infiltration was higher (P<0.01) in OP Inact-4 weeks rats than in all other groups. The present results indicate that previously trained rats that have been inactive for a while maintain higher body adiposity in response to a HFD than in freshly inactive and sedentary rats.