解偶联蛋白

摘要： 目的:基于线粒体呼吸功能,研究芪参颗粒对缺血性中风相关线粒体能量代谢障碍保护作用。方法:选用PC12神经细胞复制缺氧缺糖损伤模型,采用细胞能量代谢分析仪(Seahorse XFe 96)考察芪参颗粒及药效成分对糖氧剥夺细胞呼吸功能的保护作用。复制大鼠大脑中动脉栓塞(Middle Cerebral Artery Occlusion,MCAO)模型,采用Clark氧电极法检测芪参颗粒对MCAO大鼠脑线粒体三态呼吸速率、四态呼吸速率、磷氧比、呼吸控制率、氧化磷酸化率等呼吸功能相关指标。蛋白质印迹法(Western Blotting)检测脑线粒体功能相关解偶联蛋白(UCP)-1、UCP-2的表达水平变化。结果:芪参颗粒及其主要药效成分可提升细胞线粒体有氧呼吸水平,改善缺血性中风大鼠脑线粒体呼吸功能;与模型组比较,芪参颗粒观察组的脑组织中UCP-1、UCP-2表达明显下降(P<0.01)。结论:芪参颗粒能够显著提高缺氧后神经细胞线粒体能量代谢水平,降低缺血性脑卒中大鼠脑线粒体呼吸功能损伤,其调节作用可能与UCP密切相关。

摘要： 本研究旨在鉴定和分析甘薯(Ipomonea batatas(L.)Lam)解偶联蛋白(uncoupling protein,UCPs)基因家族成员,探究其在甘薯不同组织中的表达特异性及其对低温(4°C)、高盐(NaCl)和干旱(PEG-6000)等胁迫的响应规律。结果发现,甘薯UCP(IbUCP)含有5个家族基因,分别将其命名为IbUCP1(GenBank登录号为MW753000)、IbUCP2(GenBank登录号为MW753004)、IbUCP3(GenBank登录号为MW753001)、IbUCP4(GenBank登录号为MW753002)和IbUCP5(GenBank登录号为MW753003)。预测IbUCP的理论等电点为8.53~9.86,含有261~375个的氨基酸残基;IbUCP定位于线粒体;IbUCP为亲水蛋白,又属于线粒体载体蛋白超家族的成员,其二级结构主要包括α-螺旋和无规则卷曲,这与三级结构预测结果相符;IbUCP不存在跨膜螺旋结构和信号肽;IbUCP家族成员分为5个,与三裂叶薯和牵牛花有较近的亲缘关系,具有一定的保守性;启动子预测发现,IbUCPs基因具有基本的转录元件以及一些信号响应元件、转录因子识别结合元件和逆境等响应顺式作用元件。表达分析显示,IbUCPs基因家族成员具有组织特异性,其中IbUCP4在茎中表达最高,其余IbUCPs均在块根中最高;IbUCPs基因家族成员中响应低温胁迫的有IbUCP1、IbUCP4和IbUCP5;IbUCPs基因家族对高盐胁迫均有响应;在干旱的胁迫下,IbUCP1、IbUCP4和IbUCP5均有响应,分别在不同的时间达到峰值。多种胁迫可调控IbUCPs的表达,本研究为甘薯UCP基因的功能挖掘及甘薯抗逆品种筛选提供了一定的理论依据。

摘要： 头颈癌是发病率、死亡率均较高的癌症.现阶段治疗手段以手术、化疗、放疗为主,但对患者的治疗效果不尽理想,且并发症死亡率均较高,研究出行之有效的治疗办法刻不容缓.解偶联蛋白(UCP)是存在于体内的抗氧化系统,越来越多的研究表明抗氧化体系与诸多疾病存在关联,本综述将主要讨论解偶联蛋白与头颈癌之间的关系.

摘要： 目的 探讨腺病毒36型(Ad36)诱导分化的脂肪细胞中,长链非编码RNA(LncRNA)00602促进棕色化的可能作用.方法 根据Ad36感染与否,将肥胖患者分为Ad36阴性组和Ad36感染组.利用实时荧光定量PCR(qRT-PCR)检测2组患者网膜脂肪组织中LncRNA00602 mRNA表达水平变化,并分析其与同组患者腰臀比、收缩压、舒张压、空腹血糖、三酰甘油等指标的相关性.采用HE染色检测Ad36阴性组和Ad36感染组网膜脂肪组织中脂肪细胞大小,qRT-PCR及Western印迹法检测2组患者网膜脂肪组织中解偶联蛋白1(UCP1)、PR结构域蛋白16(PRDM16)的mRNA及蛋白质表达水平.分离、培养人脂肪源性干细胞(hADSC),利用Ad36诱导hADSC分化,并分为对照组和LncRNA00602敲低组,在敲低LncRNA00602后第0、2、4天,采用氟硼二吡咯(BODIPY)及线粒体红色荧光(Mito-Tracker Red)分别对细胞内脂滴和线粒体进行荧光染色,同时用qRT-PCR及Western印迹法检测UCP1、PRDM16表达水平的变化.结果 Ad36感染组中LncRNA00602基因表达水平高于Ad36阴性组(均P＜0.05),Ad36阴性组中LncRNA00602表达水平与以上临床指标相关性无统计学意义,而Ad36感染组LncRNA00602表达水平与血清空腹血糖、三酰甘油呈负相关(r分别为-0.522、-0.486,P＜0.05);HE染色显示,Ad36感染组平均脂肪细胞面积小于Ad36阴性组,同时UCP1、PRDM16基因表达水平均高于阴性组(均P＜0.05).在细胞水平,敲低LncRNA00602后第2、4天,LncRNA00602敲低组脂肪细胞的脂滴面积大于对照组,同时线粒体数量较对照组减少,差异均有统计学意义(P＜0.05或P＜0.01);与对照组相比,LncRNA00602敲低组脂肪细胞棕色化标志基因UCP1、PRDM16mRNA和蛋白质表达水平均显著降低(均P＜0.05).结论 Ad36诱导的脂肪细胞分化中,LncRNA00602可能正向调控了 UCP1、PRDM16的表达和脂滴的代谢变化,并引起脂肪细胞棕色化的发生.

摘要： Background Researches showed that elevatory blood glucose level results in long-term damage of cells and tissue,or metabolic memory phenomenon,and manipulation of hyperglycemic memory is a good approach in the prevention of diabetic complications.However,its mechanism is not clear.It is speculated that the pathogenesis of diabetic retinopathy (DR) in diabetic patients may be associated to related mechanisms.Uncoupling proteins (UCPs) can decrease the production of reactive oxygen species (ROS),which may be related to DR.Objective This study was to explore the association between DR and the single nucleotide polymorphisms (SNPs) of UCP genes in Chinese Han population with type 2 diabetes.Methods A cross-sectional study was performed.This study was approved by Ethic Committee of Affiliated First Hospital of Shanghai Jiao Tong University and complied with Declaration of Helsinki,and written informed consent was obtained from each subject prior to any medical examination.One thousand eight hundreds and seventy-five patients with type 2 diabetes mellitus were enrolled in Xinjing district of Shanghai city by cluster sampling from November 2014 to January 2015.The demographic and medical baseline characteristics,ocular examination and laboratory tests were obtained and periphery blood of 2 ml was collected for extraction of DNA.Eight tag SNPs of UCP1,three tag SNPs of UCP2,and seven tag SNPs of UCP3 were selected as marker locus for the detection of genotype by Sequenom Mass ARRAY.Matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry platform were used for genotyping.Hardy-Weinberg equilibrium (HWE) analysis,allele and genotype frequencies,haplotype analysis,and association tests for DR and SNPs were performed by SAS and SHEsis software.Results A total of 530 DR patients were checked out from 1 875 subjects with type 2 diabetes mellitus,with the detection rate of 28.27％.rs660339 locn of UCP2 gene and rs1626521,rs668514 locus of UCP3 gene appeared to have low detectable rates,and the secondary allele base frequency of rs632862 in UCP2 gene was ＜0.01 and rs15763 of UCP3 gene was unmatched with HWE,therefore,these locus analysis was not included.In 13 SNPs locus included in the analysis,only 2 SNPs of UCP1 gene were related to DR.Compared with the non-diabetic retinopathy (NDR) patients,the G allele frequency of rs10011540 was increased (P =0.03,OR =1.31,95 ％ confidence interval[CI] =1.03-1.67,and T allele frequency of rs3811787 was decreased (P=0.04,OR=0.86,95％ CI=0.75-0.99) in DR patients.Genotyping detection showed that the C/C and A/A frequencies of rs3811790 in UCP1 gene were significantly more and C/A frequency was less in DR patients than those in NDR patients (all at P＜0.01).The logistic regression analysis indicated an association of SNPs of rs10011540 and rs3811787 with DR independent from glucose and disease duration.Conclusions The SNPs of rs10011540 and rs3811787 locus in UCP1 gene are associated with DR in Chinese type 2 diabetes patients.%背景 研究发现血糖水平的短期升高可对细胞和组织造成长期损害,这种损伤可能存在代谢记忆现象,合理管理血糖代谢记忆对糖尿病并发症的预防有重要作用,但其机制尚未完全阐明,推测糖尿病患者中糖尿病视网膜病变(DR)的发生可能与相关机制有关.解偶联蛋白(UCPs)可减少线粒体活性氧(ROS)的生成,可能与DR发病相关. 目的 探讨中国汉族2型糖尿病人群中DR与UCP基因单核苷酸多态性(SNPs)之间的关系.方法 采用横断面研究方法和整群抽样法,于2014年11月至2015年1月在上海市新泾社区对1 875例确诊为2型糖尿病的患者进行流行病调查,收集受检者的基本信息、眼科检查和血生物化学检验结果,采集每例患者的全血2 ml以提取DNA.采用Sequenom平台将UCP1基因的8个SNPs位点、UCP2基因的3个SNPs位点及UCP3的7个SNPs位点选为标记位点以检测基因型,采用SAS和SHEsis软件计算Hardy-Weinberg平衡、碱基型和基因型频率,评估各位点SNPs与DR之间的关系. 结果 受检的1 875例2型糖尿病患者中530例患DR,占28.27％.UCP2基因的rs660339位点和UCP3基因的rs1626521位点、rs668514位点的检出率低,UCP2基因rs632862位点次要等位碱基频率＜0.01,UCP3基因的rs15763位点不符合Hardy-Weinberg平衡,故均不纳入分析.在纳入分析的13个SNPs位点中,仅有UCP1基因的2个SNPs位点与DR发病有关,其中与非糖尿病视网膜病变(NDR)患者比较,DR患者rs10011540的G碱基频率增加[P=O.03,OR=1.31,95％可信区间(C1)=1.03～1.67],rs3811787的T碱基频率下降(P=0.04,OR=0.86,95％ CI=0.75 ～0.99).基因型分析发现,DR患者UCP1基因的rs3811790位点纯合子C/C和A/A频率明显多于NDR患者,杂合子C/A频率少于NDR患者,差异均有统计学意义(P＜0.01).Logistic回归分析提示,在排除了血糖水平和糖尿病病程的影响因素后,rs10011540和rs3811787位点SNPs仍是DR发病的独立影响因素.结论 中国汉族2型糖尿病患者UCP1基因rs10011540和rs3811787位点SNPs与DR发病相关.

摘要： 目的 为进一步揭示热性中药的分子机制、诠释中药寒热药性理论的科学内涵,同时对能量代谢开关解偶联蛋白亚型1(UCP1)的表达调控作用进行研究.方法 采用热偶技术对小鼠的核心温度和尾部皮肤温度进行了给药后的实时监测,温度的采集分析采用了热偶检测技术,UCP1的表达量分别采用了荧光定量PCR和Western blot的技术.结果辣椒碱给药后小鼠机体中心温度先降低后上升,尾部皮肤温度以升高为主,与空白对照组相比差异有显著性(P<0.05或P<0.01);UCP1的基因和蛋白的表达量均明显上调(P<0.05或P<0.01).结论 上调UCP1 的表达进而提高机体的能量代谢可能是辣椒碱作为辣椒的热性成分表征热性属性的生物分子机制之一.%Aim Tofurtheruncoverthemolecular mechanism of hot herbs and thus to decode the scientif-ic significance of herb nature theory,real-time check on the core body temperature and tail skin temperature of the capsaicin-administrated mice was conducted and the expression of UCP1 at the mRNA and protein levels wasalsoperformed.Methods Thetemperaturesof the mice were registered by the heat electronic couple technique,and the expression of UCP1 was assayed by the methods real-time PCR and Western blot respec-tively.Results Thecorebodytemperatureofthe mice after administration of capsaicin decreased andthen increased, while the tail skin temperature in-creased rapidly upon treatment with capsaicin (P <0. 05 or P<0. 01 );both the mRNA and protein ex-pression levels of UCP1 were up-regulated(P<0. 01). Conclusion Promotiononenergymetabolismthough up-regulation of UCP1 may be one of the biologically molecular mechanisms for the capsaicin to demonstrate its characteristics in terms of cold-hot natures of Chi-nese herbs.

摘要： 目的 观察胃旁路术(Roux-en-Y,RYGB)后T2DM模型大鼠肩胛棕色脂肪组织(brown adipose tissue,BAT)形态、功能及特异表达解偶联蛋白(uncoupling protein,UCP1)改变,探索RYGB对T2DM模型大鼠BAT的影响及其相关机制,为RYGB治疗T2DM患者提供理论及实验依据.方法 SD大鼠经高脂高糖饲料喂养2周后,于大鼠腹腔内注射链脲佐菌素(streptozocin,STZ)30 mg/kg进行造模,72 h和1周后快速血糖仪测随机血糖,2次均≥16.7 mmol/L为成功造模,成模大鼠饲养环境:单笼饲养,标准大鼠饲料喂养,自然昼夜循环,室内温度(18±2)°C,室内湿度(50±2)％.动物分组:成模大鼠随机选取50只,以随机数字表法按干预方式分为糖尿病手术组(A组,n=10),行保留全胃的RYGB手术;糖尿病假手术组(B组,n=10),麻醉方法及切口同RYGB组,手术方式为胃前壁切开再缝合、空肠相应位置切断后原位吻合,缝合方法同糖尿病手术组;糖尿病对照组(C组,n=10),建立糖尿病造模成功后正常饲料喂养;健康对照组(D组,n=10),无特殊处理,保证充足饮水.其余大鼠备用.术前及术后第1、2、4、8周分别测各组大鼠体质量(body mass,BM)、空腹血糖(fasting plasma insulin,FPG)、空腹血清胰岛素(fasting plasma insulin,Fins).截面棕色脂肪细胞平均半径和细胞数目,利用IPP6.0图像分析软件辅助计算截面细胞数,进一步计算脂肪细胞平均半径;运用Western blot的方法进行检测UCP1表达.结果 ①糖尿病大鼠较健康对照组SD大鼠空腹血糖、空腹血清胰岛素水平及体质量增高,胰岛素敏感指数显著降低.②HE染色结果显示:糖尿病手术组(A组)大鼠较糖尿病对照组(C组)及糖尿病假手术组(B组)大鼠的截面细胞数及棕色脂肪平均半径明显增高,差异有统计学意义(P＜0.01),糖尿病手术组(A组)大鼠与健康对照组(D组)大鼠,糖尿病对照组(C组)大鼠与假手术组(B组)大鼠间比较差异无统计学意义(P＞0.05).③Western blot结果显示:胃旁路术后糖尿病手术组(A组)大鼠较糖尿病假手术组(B组)、糖尿病对照组(C组)大鼠肩胛棕色脂肪组织对UCP1表达显著增加(P＜0.05),糖尿病假手术组(B组)与糖尿病对照组(C组)及糖尿病手术组(A组)与健康对照组(D组)之间比较差异无统计学意义(P＞0.05).结论 RYGB能在降低糖尿病大鼠BM及胰岛素抵抗(insulin resistance,IR)的同时也促进大鼠肩胛BAT对UCP1的表达.RYGB可能通过调节UCP1信号通路的途径增加体内BAT活性实现改善机体IR.%Objective To observe what changes the brown adipose tissue (BAT) of T2DM rat models would have,including morphology,function and specially expressed uncoupling protein (UCP1) after the gastric bypass (Roux-en-Y,RYGB) and to explore the effects of RYGB on BAT of T2DM rat models and its related mechanism in order to provide a theoretical and experimental basis for treatment of T2DM patients with RYGB.Methods SD rats were given a high-fat and high-sugar diet for two weeks,by injecting streptozotocin (STZ) 30 mg/kg intraperitoneally to build models.Blood glucose was measured after 72 h and 1 week by the fast blood glucose meter.The models were built successfully if blood glucose at both times were ≥ 16.7 mmol/L.Feeding environment:individually caged,standard rat feed,natural circadian cycle,indoor temperature (18±2)°C,indoor humidity (50±2)％.50 rats were randomly selected and dividing into four groups according to intervention methods:diabetes operation group (group A,n=10),undergoing RYGB surgery with the whole stomach kept;diabetes sham operation group (group B,n=10),the same anesthesia and incision as the previous RYGB group.The operation mode was anterior gastric wall incision and suture,jejunum transection in corresponding position and in situ anastomosis with the same suture method as group A;diabetes control group (group C,n=10),normally feeding after building models;and the last one was the healthy control group (group D,n=10):no special treatment,adequate water feeding ensured.The rest of rats remained to be used.The body mass (BM),fasting blood glucose (FBG),fasting serum insulin(Fins)before and at the 1st,2nd,4th and 8th week after surgery were measured.The number of transversal ceils was calculated by IPP6.0 image software and the average radius of fat cells was calculated.UCP1 expression was tested with western blot.Results ① The fasting blood glucose,fasting serum insulin level and the body weight of dia betic rats were higher than those of the control group,but the insulin sensitivity index was significantly lower.② HE Staining showed:diabetes operation group (group A) rats,compared with diabetes control group and diabetes sham operation group(group B),had obviously higher brown fat cell counts transversally and average radius,and the difference was statistically significant (P＜0.01).Diabetes operation group (group A) rats had no significant difference from the healthy control group(group D) rats,and the diabetes control group (group C) rats had no significant difference from sham operation group (group B) rats as well.③ Western blot showed that after the gastric bypass surgery,compared with the diabetes sham operation group (group B) and the diabetes control group (group C),UCP1 expression of brown adipose tissue of the diabetes operation group (group A) increased significantly (P＜0.05).The diabetes sham operation group (group B) had no significant difference from the diabetes control group (group C),and the diabetes operation group(Group A) had no significant difference from the healthy control group (Group D) as well (P＞0.05).Conclusion RYGB can reduce the body mass and insulin resistance (IR) of diabetic rats and,at the same time,promote the expression of UCP1 of brown adipose tissue.RYGB might increase the activity of brown adipose tissue by regulating the UCP1 signaling pathway to improve body's insulin resistance.

摘要： 肥胖、代谢综合症、Ⅱ型糖尿病等代谢系统疾病,经常导致线粒体呼吸复合物中活性氧(ROS)生成增加,进而导致脂肪在心肌细胞、脂肪细胞、骨骼肌、肝细胞中积累.动物实验表明,在心肌细胞中,脂质积累会产生脂毒性,从而进一步导致细胞凋亡、心脏衰竭.因此,心肌细胞等通过高表达解偶联蛋白(UCP)来进行抗氧化应激和脂毒性适应.在肥胖的啮齿类动物和人类心脏中,UCP2和UCP3通过下调细胞程序死亡,使心肌细胞免于死亡以致心力衰竭.UCP激活后通过减少ROS的生成和细胞凋亡,影响细胞色素c和促凋亡蛋白的释放.本综述简要总结了UCP如何通过抗ROS生成及维持生物能量代谢平衡来起到保护心肌细胞、保护心脏的作用.%Metabolic diseases such as obesity,metabolic syndrome,and type Ⅱ diabetes are often characterized by increased reactive oxygen species(ROS) generation in mitochondrial respiratory complexes,associated with fat accumulation in cardiomyocytes,skeletal muscle,and hepatocytes.Several rodents studies showed that lipid accumulation in cardiac myocytes produces lipotoxicity that causes apoptosis and leads to heart failure,a dynamic pathological process.Meanwhile,several tissues including cardiac tissue develop an adaptive mechanism against oxidative stress and lipotoxicity by overexpressing uncoupling proteins(UCP).In heart from rodent and human with obesity,UCP2 and UCP3 may protect cardiomyocytes from death and from a state progressing to heart failure by down-regulating programmed cell death.UCP activation may affect cytochrome c and proapoptotic protein release from mitochondria by reducing ROS generation and apoptotic cell death.Therefore the aim of this review is to discuss recent findings regarding the role that UCP play in cardiomyocyte survival by protecting against ROS generation and maintaining bioenergetic metabolism homeostasis to promote heart protection.

摘要： Objective To investigate the effect of hypobaric hypoxia and cold exposure on brown adipose tissue in mice. Methods Twenty-four 6-week old SPF C57BL/6 male mice were randomly divided into 4 groups with 6 mice in each group: normal atmospheric pressure and temperature group ( 18~22°C, 20~60 m ) ( NTNP ) , low atmospheric pressure and normal temperature group ( 18~22°C, altitude of 5000 m ) ( NTLP ) , normal atmospheric pressure and cold exposure group(0~6°C, altitude of 20 ~60 m)(LTNP), low atmospheric pressure and cold exposure group(0 ~6°C, altitude of 5,000 m)(LTLP). The experimental period was 4 weeks. The body weight was measured at the beginning and end of the experiment. By the end of the four-week trial, the back and inguinal fat were dissected and observed by histology using HE staining. The expression of UCP-1 as the marker of brown adipose tissue in the back fat was detected by qPCR and western blot. Results The body weight gain of NTNP group was higher ( P< 0. 05 ) than the other three groups. Meanwhile, the color of the back and groin fat tissue of mice of LTNP and LTLP groups were darker, the blood supply in mice of these two groups was richer than the NTLP group. The volume of adipose tissue of NTNP group was higher than others. The histology showed that the back adipose cells of the mice were smaller and darker and full of multilocular lipid droplets, exhibiting a typical morphology of brown fat cells. Compared with the NTNP and NTLP groups, the mRNA and protein levels of UCP-1 were higher under cold exposure, while low atmospheric pressure had a tendency to reduce the mRNA expression of UCP-1. Conclusions The formation of brown fat is affected by the imitated conditions of low atmospheric pressure and cold exposure, and is more closely related to the decresed temperature.%目的 探索低温低压环境对小鼠褐色脂肪组织的影响.方法 选取个体健康均一的6周龄成年雄性C57BL/6 N小鼠24只,平均分为4组,每组6只鼠,分别饲养在常温常压(18~22°C、海拔20~60 m)、常温低压(18~22°C、海拔5000 m)、常压低温(0~6°C、海拔20~60 m)、低温低压(0~6°C、海拔5000 m)的环境中.实验周期为4周,在试验开始和结束时分别测量每只小鼠的体重,在实验结束后完整取下试验小鼠背部及腹股沟脂肪,并对背部及腹股沟脂肪组织进行HE染色,对背部脂肪的褐色脂肪的标志物UCP-1进行qPCR分子表达及western blot蛋白表达的测定.结果 低温低压、低温常压和常温低压组小鼠的体重增加量显著低于同期正常对照组小鼠;低温低压、低温常压小鼠背部和腹股沟脂肪组织颜色较深,血运丰富,常温常压组的脂肪组织形态较其他组偏大;染色结果显示小鼠背部脂肪细胞充盈多个脂肪泡,细胞较小,颜色较深,形态上是典型的褐色脂肪细胞;在低温条件下,小鼠背部脂肪组织的褐色脂肪标志物UCP-1在mRNA和蛋白水平上高表达,低压条件下仅在mRNA的水平上有上调.结论 模拟高原环境的低温低压条件对小鼠褐色脂肪组织的形成有刺激作用,这种作用更多的与温度的降低有关.

摘要： 热能和生物能ATP是机体所需能量的二种形式，它们符合中医阴阳学说“阴”“阳”这一对范畴.ATP为阴，热能为阳，二者构成机体能量的阴阳平衡.解偶联蛋白基因表达出的解偶联蛋白，具有调节热能和ATP生成，调节机体能量平衡的作用，推测解偶联蛋白基因可能是一种调控机体阴阳平衡的基因.

摘要： 解偶联蛋白(UCPs)是存在于线粒体内膜上重要的转运蛋白,基于其功能,解偶联蛋白基因被视为肥胖病及2型糖尿病的重要候选基因.解偶联蛋白5(uncoupling protein 5,UCP5)是解偶联蛋白家族的新成员,与组织特异性的温度调节和代谢调节有关,本文是针对UCP5与机体的能量代谢和体温调节的相关研究进行讨论.

摘要： 鸡肉质风味已成为育种工作者研究的一个重要方向，利用候选基因遗传标记在基因水平上找到影响肉质风味性状的主效基因或连锁基因，从而应用于鸡肉质风味的育种改良是育种工作者适应当前人们对肉质风味要求亟待开展并完善的工作。本文综述了与肌内脂肪及肌苷酸合成相关的解偶联蛋白(UCP)、脂蛋白脂酶(LPL)、腺苷琥珀酸裂解酶(ADSL)、腺苷一磷酸脱氨酶(AMPD)和PURH 5种基因研究进展，以期为分子育种提供参考。

摘要： 肌内脂肪是影响肉品质量和风味的一个重要因素，肌内脂肪含量高，肉品的质量和风味就好。脂肪的代谢与多种酶相关，本文综述了与肌内脂肪合成代谢相关的脂蛋白脂酶(LPL)、脂肪酸结合蛋白(FABP)、瘦蛋白受体(OBR)、解偶联蛋白(UCP)基因的研究进展。

摘要： 目的：探讨六味地黄丸对左旋甲状腺素所致甲亢小鼠解偶联蛋白-2、3基因表达的影响。rn 方法：昆名种小鼠36只，随机分为空白组、甲状腺功能亢进(甲亢)组和甲亢+六味地黄丸组，利用左旋甲状腺素致小鼠甲亢；用半定量逆转录聚合酶链反应(RT-PCR)，检测各组别小鼠脂肪组织UCP2与肌肉组织UCP3 mRNA的表达水平。并测定六味地黄丸对甲亢小鼠的体重、T3、T4、ATPasc、MDA、SOD的影响.rn 结果：与空白组相比较，甲亢组的解偶联蛋白-2、3基因表达显著增加；而甲亢+六味地黄丸组的解偶联蛋白-2、3基因表达比甲亢组显著下降。六味地黄丸还显著增加左旋甲状腺素所致甲亢小鼠的体重，提高血液ATPase和SOD活性，降低血清T3、T4含量，降低肝组织MDA含量.rn 结论：六味地黄丸可以下调左旋甲状腺素所致甲亢小鼠解偶联蛋白-2、3基因的表达.显著改善左旋甲状腺素所致甲亢小鼠的甲亢作用。

摘要： 解偶联蛋白(uncoupling proteins，UCPs)是线粒体内膜上参与质子转运的蛋白质，可将呼吸链中ATP产生过程解偶联，导致能量以热的形式消耗掉，以减少能量蓄积。大量研究发现，UCP2与肥胖和糖尿病发生有着密切关联。为进一步研究UCP2与肥胖之间的关系，本研究以3T3-L1前体脂肪细胞为研究对象，通过诱导分化，用不同浓度的葡萄糖处理体外培养的3T3-L1脂肪细胞，观察其UCP2mRNA表达水平的变化。

摘要： 报道从一个地中海海绵（Ｒｅｎｉｅｒａ ｓｐ．）中发现了一个具有全新笼状骨架的新型海洋大环生物碱，这个化合物被命名为米寒宁（Ｍｉｓｅｎｉｎｅ）。初步的生物活性实验表明该化合物具有显著的抗癌活性（抗ＫＢ细胞ＩＣ〈，５０〉１ｍｇ／ｍＬ）。作者通过深入仔细的光谱学、化学方法将其结构确定为ｌ／ｌａ。该论文还报道了这一新化合物的可能的生源合成途径。

摘要： 报道从一个地中海海绵（Ｒｅｎｉｅｒａ ｓｐ．）中发现了一个具有全新笼状骨架的新型海洋大环生物碱，这个化合物被命名为米寒宁（Ｍｉｓｅｎｉｎｅ）。初步的生物活性实验表明该化合物具有显著的抗癌活性（抗ＫＢ细胞ＩＣ〈，５０〉１ｍｇ／ｍＬ）。作者通过深入仔细的光谱学、化学方法将其结构确定为ｌ／ｌａ。该论文还报道了这一新化合物的可能的生源合成途径。

摘要： 报道从一个地中海海绵（Ｒｅｎｉｅｒａ ｓｐ．）中发现了一个具有全新笼状骨架的新型海洋大环生物碱，这个化合物被命名为米寒宁（Ｍｉｓｅｎｉｎｅ）。初步的生物活性实验表明该化合物具有显著的抗癌活性（抗ＫＢ细胞ＩＣ〈，５０〉１ｍｇ／ｍＬ）。作者通过深入仔细的光谱学、化学方法将其结构确定为ｌ／ｌａ。该论文还报道了这一新化合物的可能的生源合成途径。

摘要： 报道从一个地中海海绵（Ｒｅｎｉｅｒａ ｓｐ．）中发现了一个具有全新笼状骨架的新型海洋大环生物碱，这个化合物被命名为米寒宁（Ｍｉｓｅｎｉｎｅ）。初步的生物活性实验表明该化合物具有显著的抗癌活性（抗ＫＢ细胞ＩＣ〈，５０〉１ｍｇ／ｍＬ）。作者通过深入仔细的光谱学、化学方法将其结构确定为ｌ／ｌａ。该论文还报道了这一新化合物的可能的生源合成途径。

摘要： 解偶联剂促进污泥解偶联效果的诊断方法，它涉及一种解偶联效果的诊断方法。本发明是为了解决现有方法诊断不能直接表示微生物体内的解偶联效果的技术问题。方法如下：将一部分污泥混合液混合均匀，加入三氯乙酸溶液超声，得匀质混合液；取匀质混合液并加入缓冲溶液混合；过滤；测定滤液荧光强度；测定剩余待测溶液的污泥浓度；将荧光强度除以污泥浓度，得到比ATP浓度；通过比ATP浓度的大小诊断污泥的解偶联效果，当比ATP浓度小于60RLU·L/mg时，污泥体内的ATP合成收到明显抑制，发生代谢解偶联。本发明可以适用于判定不同解偶联剂对污泥内解偶联促进效果，其测定方法简单准确。本发明属于解偶联剂解偶联效果的诊断领域。

摘要： 本发明属于重组生物技术领域，特别属于蛋白质表达领域。本发明一般涉及在生产过程中提高细菌宿主细胞的目的蛋白质的表达水平的方法。本发明特别涉及通过在生产过程中表达抑制细菌宿主细胞生长的噬菌体蛋白质来提高细菌宿主细胞表达目的蛋白质的能力。在生产过程中使制造目的蛋白质的细菌宿主细胞的生长解偶联减少(i)代谢负担，(ii)氧需求，(iii)代谢热发展，和(iv)避免由异源蛋白质表达引起的应激反应，由此提高宿主细胞产生目的蛋白质的能力。本发明还涉及宿主细胞在蛋白质表达、细胞培养技术中的用途，更具体地涉及培养宿主细胞以产生目的蛋白质。

摘要： 本发明涉及调节解偶联蛋白2(UCP2)的表达和/或功能的反义寡核苷酸，尤其是，通过靶向解偶联蛋白2(UCP2)的天然反义多核苷酸。本发明还涉及这些反义寡核苷酸的鉴定和它们在治疗UCP2表达相关的疾病和病症中的用途。

摘要： 本发明提供了一种褐色脂肪组织中解偶联蛋白‑1分离纯化的方法，通过将试验动物的褐色脂肪组织用提取液A混合研磨，离心去上层脂肪，取一次上清液；将所述一次上清液离心去沉淀，取二次上清液；将二次上清液离心取一次沉淀，将一次沉淀与提取液B混匀，20 kHz条件下超声处理，将超声后的溶液离心取二次沉淀；将二次沉淀与提取液B混匀，加入TritonX‑100混匀，20 kHz条件下超声处理，将超声后的溶液在离心取三次上清液；将三次上清液装柱、洗脱纯化，得到解偶联蛋白‑1。本发明的纯化效果较好，成本低，非常适合实验室采用。

摘要： 本发明公开了一种敲入有解偶联蛋白1-荧光素酶基因的非人哺乳动物模型及其构建方法和应用。本发明构建的敲入有解偶联蛋白1-荧光素酶的非人哺乳动物模型可作为白色脂肪细胞褐色化的药物的筛选平台，可实现简单，迅速，大规模的筛选调控UCP1表达的药物；可以在不伤害非人哺乳动物的前提下，利用荧光成像仪直接活体检测UCP1的表达和分布。

摘要： 本发明提供了一种褐色脂肪组织中解偶联蛋白-1分离纯化的方法，通过将试验动物的褐色脂肪组织用提取液A混合研磨，离心去上层脂肪，取一次上清液；将所述一次上清液离心去沉淀，取二次上清液；将二次上清液离心取一次沉淀，将一次沉淀与提取液B混匀，20kHz条件下超声处理，将超声后的溶液离心取二次沉淀；将二次沉淀与提取液B混匀，加入TritonX-100混匀，20kHz条件下超声处理，将超声后的溶液在离心取三次上清液；将三次上清液装柱、洗脱纯化，得到解偶联蛋白-1。本发明的纯化效果较好，成本低，非常适合实验室采用。

摘要： 本发明公开了一种敲入有解偶联蛋白1-荧光素酶基因的非人哺乳动物模型及其构建方法和应用。本发明构建的敲入有解偶联蛋白1-荧光素酶的非人哺乳动物模型可作为白色脂肪细胞褐色化的药物的筛选平台，可实现简单，迅速，大规模的筛选调控UCP1表达的药物；可以在不伤害非人哺乳动物的前提下，利用荧光成像仪直接活体检测UCP1的表达和分布。

摘要： 本发明涉及调节解偶联蛋白2(UCP2)的表达和/或功能的反义寡核苷酸，尤其是，通过靶向解偶联蛋白2(UCP2)的天然反义多核苷酸。本发明还涉及这些反义寡核苷酸的鉴定和它们在治疗UCP2表达相关的疾病和病症中的用途。

摘要： 本发明属于生物技术领域。具体涉及虎斑颈槽蛇肌肉解偶联蛋白－SA(uncoupling protein－snake A，UCP－SA)分子克隆。本发明应用简并引物和3’，5’－RACE首次从虎斑颈槽蛇肌肉中克隆了UCP－SA基因。UCP与多种疾病相关。如，糖尿病、心血管疾病以及肿瘤。因此，以UCP作为靶点，可以制备治疗这些疾病的药物。

摘要： 本发明属于生物技术领域。具体涉及虎斑颈槽蛇肌肉解偶联蛋白(uncoupling protein－snake B，UCP－SB)分子克隆。本发明应用简并引物和3′，5′－RACE首次从虎斑颈槽蛇肌肉中克隆了UCP－SB基因。UCP与多种疾病相关。如，糖尿病、心血管疾病以及肿瘤。因此，以UCP作为靶点，可以制备治疗这些疾病的药物。