胰岛素样生长因子-I的研究进展

哺乳动物胰岛素样生长因子(IGF-I)是介导生长激素促生长效应的主要因子,本文对IGF-I的结构、结合蛋白类型、受体及其在机体中的生物功能和影响因素等作了阐述,并分析了IGF-I在动物生产中的应用前景.     

运动对大鼠骨骼肌及血清GH,IGF-I水平研究

生长激素(GH)、胰岛素样生长因子I(IGF-I)都是了解GH-IGF轴变化的主要指标。IGF不仅是内分泌因子,还能在组织局部起作用。通过对6周递增负荷跑台练习的大鼠进行研究,结果显示:运动后即刻处死的大鼠血清GH水平明显升高(P<0.01);运动组与对照组相比,骨骼肌IGF-I水平有明显升高(P<0.01),表明运动对骨骼肌组织内IGF的分泌有调节作用。     

血管内皮生长因子在低氧运动中的效应及一氧化氮的介导作用

血管内皮生长因子(VEGF)是内皮细胞特异性的有丝分裂原,具有促进内皮细胞增生、迁移和增加血管通透性等多种重要生物学作用。研究表明,VEGF在发挥这些生物学作用的过程中一氧化氮(NO)起着必不可少的作用。随着高原训练理论研究的不断深入,低氧运动条件下VEGF对机体机能影响的研究倍受关注,其中VEGF和NO关系的探讨有助于低氧运动状况下对VEGF作用机制的进一步阐述。     

体育运动中的间歇性低氧训练研究

从间歇性低氧训练的产生及其在运动训练中的应用和生理、生化机制等方面进行综述，旨在促进间歇性低氧训练在运动训练中进一步应用．     

高原低氧运动对机体Hb及Hb和O2亲和力的影响

采用文献资料法，研究了高原低氧环境及运动对人体Hb及Hb与O2亲和力的影响，对提高有氧运动代谢能力以及运动成绩有良好的效果。为运动员进行高原训练，提供科学依据。     

IGF-I、OPN、PTEN蛋白在非小细胞肺癌中的表达及其意义

探讨胰岛素样生长因子1(IGF-I)、骨桥蛋白(OPN)和PTEN在人非小细胞肺癌中的表达及其相关性,并分析其与非小细胞肺癌的关系。应用免疫组织化学SP法检测61例肺癌组织和30例癌旁组织中IGF-I、OPN、PTEN的表达情况。结果显示,①肿瘤组织中IGF-I、OPN蛋白表达显著高于癌旁组织(P<0.05),IGF-I的表达与肿瘤分化程度、淋巴结转移有关(P<0.05),OPN的表达与患者肿瘤分化程度、淋巴结转移、TNM分期有关(P<0.05),肿瘤组织中PTEN蛋白表达明显低于癌旁组织(P<0.05),PTEN的表达与肿瘤大小、肿瘤组织的分化程度、有无淋巴结转移有关(P<0.05)。②IGF-I的表达与OPN的表达呈正相关(P<0.05),IGF-I、OPN与PTEN的表达呈负相关(P<0.05)。研究表明,IGF-I、OPN、PTEN蛋白与非小细胞肺癌的发生发展密切相关,三者的表达对判断肺癌恶性程度和预后具有参考意义。     

肥胖大鼠低氧训练中羟自由基与胰岛素抵抗相关性研究

为明确不同模式的低氧训练对肥胖大鼠自由基代谢的影响，探讨低氧训练过程中自由基代谢与胰岛素敏感性的关系，构建肥胖大鼠模型，进行4周的低氧训练干预，定期称量，实验末称量并统计其体脂，测定血清胰岛素、血糖、羟自由基和过氧化氢酶水平，统计各实验组胰岛素抵抗指数。实验结果表明，低氧暴露有利于机体胰岛素敏感性的提高，抗氧化酶的活性的降低可能与机体胰岛素敏感性有一定关系。     

低氢、运动及低氢训练对肝细胞凋亡影响的研究进展

低氧与健康的研究是近年来临床医学、环境医学、航空航天医学和运动医学的研究重点问题之一。从肝细胞凋亡的角度研究运动对肝细胞的影响及其与运动性疲劳之间的关系,对科学制定训练计划等具有重要的意义。低氧训练使机体处于更加缺血和缺氧状态,血液的重新分配,使肝脏出现暂时的缺血,运动强度降低后血液重新回流形成血液再灌注,导致肝损伤,诱导细胞凋亡。细胞凋亡的过低或过高都导致疾病的发生。肝细胞凋亡的异常在急、慢性肝损伤的发病机制中起着重要的作用。就有关低氧、运动及低氧训练对肝细胞凋亡的影响,引起凋亡发生的基因调控及机制进行相关综述。     

间歇性低氧及运动对大鼠红细胞膜Na+-K+-ATP酶和Ca2+-Mg2+-ATP酶活性的影响

Wistar雄性大鼠分为常氧对照组、常氧运动组、低氧对照组、低氧运动组.分别对常氧运动、低氧运动组进行游泳训练,对低氧对照、低氧运动组进行低氧刺激.用导管法测血压和心率,用比色法测红细胞膜Na+-K+-ATP酶Ca2+-Mg2+-ATP酶活性,探讨低氧和训练对红细胞膜Na+-K+-ATP酶和Ca2+-Mg2+-ATP酶活性的影响.发现低氧刺激降低大鼠红细胞膜Na+-K+-ATP酶和Ca2+-Mg2+-ATP酶的活性,而适宜负荷运动则可提高以上两种酶的活性.结果表明,间歇性低氧运动对大鼠红细胞膜的Na+-K+-ATP酶和Ca2+-Mg2+-ATP酶活性具有一定的保护作用.     

IGF-I、HGF、TGF-β1、IFN-γ对奶牛乳腺上皮细胞增殖活性的影响

研究胰岛素样生长因子-I(IGF-I)、肝细胞生长因子(HGF)、转化生长因子β1(TGF-β1)、干扰素-γ(IFN-γ)对奶牛乳腺上皮细胞体外增殖的调节作用。应用组织块培养和差速消化法获取原代奶牛乳腺上皮细胞,免疫荧光鉴定正确后MTT法评价不同浓度的4种细胞因子对奶牛乳腺上皮细胞体外增殖的影响。IGF-I、HGF分别在10~200 ng/m L,0.1~100 ng/m L浓度范围内对乳腺上皮细胞的增殖呈正相关。而TGF-β1(2.5~100 ng/m L)、IFN-γ(5~160 ng/m L)则剂量依赖性地抑制乳腺上皮细胞增殖。IGF-I、HGF均能促进奶牛乳腺上皮细胞的体外增殖,该作用在一定浓度范围内有剂量依赖性;TGF-β1、IFN-γ对乳腺上皮细胞的增殖作用出现剂量抑制效应。该研究为下一步深入探讨细胞因子对奶牛泌乳机制的研究奠定基础。     

Growth restoration of insulin-deficient diabetic rats by recombinant human insulin-like growth factor I

Insulin-like growth factor I (IGF-I) and insulin stem from a common precursor, are structural homologues, act through similar receptors and elicit insulin-like and growth-promoting effects in vitro and in vivo. Serum IGF-I levels are controlled by growth hormone, insulin and nutrition. Insulin-deficient growth-arrested diabetic animals have reduced serum IGF-I levels which are restored towards normal by insulin but not by growth-hormone treatment. Here we show that normal growth of diabetic rate is restored by infusion of recombinant human (rh)IGF-I without normalization of the blood sugar level and that insulin acts via an increase of IGF-I synthesis on growth of diabetic rats. We describe a new mechanism of endocrine control of growth in which IGF-I is the major stimulator at the cellular level. Growth hormone and insulin act mainly by modulating the hepatic synthesis of IGF-I.     

Stimulation of tyrosine-specific phosphorylation in vitro by insulin-like growth factor I

Several mitogens elicit tyrosine-specific protein kinase activities. Although the physiological significance of this is unclear, the generality of these reactions implies that this may be an inherent feature of growth factor-growth factor receptor interactions. The observed mitogenic properties of the polypeptide insulin-like growth factor I (IGF-I) indicated that it might also stimulate such activity. We report here that IGF-I stimulates a tyrosine-specific protein kinase in a time- and dose-dependent fashion. The close correspondence between an approximate 50% effective dose (ED50) of phosphorylation and an approximate Kd for IGF-I binding leads us to conclude that a high-affinity IGF-I receptor, not the structurally similar insulin receptor, is the mediator of IGF-I stimulated kinase activity. Immunoprecipitation indicates that both the beta-subunit of the IGF-I receptor and the beta-subunit of the insulin receptor are targets for the IGF-I-stimulated protein kinase.     

Human chromosomal mapping of genes for insulin-like growth factors I and II and epidermal growth factor

Many of the actions previously attributed to pituitary-derived growth hormone are mediated by polypeptide growth factors. These include the insulin-like growth factors I and II (IGF-I and IGF-II), which are members of the insulin family of proteins. We report here the chromosomal mapping of the human genes for IGF-I and IGF-II. IGF-II maps to the short arm of chromosome 11, which also contains the gene for insulin and the proto-oncogene c-Ha-ras1 (ref. 9). IGF-I maps to chromosome 12, which is evolutionarily related to chromosome 11 and carries the gene for the proto-oncogene c-Ki-ras2 (refs 10,44). We have also localized the human gene for an unrelated polypeptide hormone, epidermal growth factor, to chromosome 4q, in the same region as another specialized growth factor, T-cell growth factor. We speculate that these map assignments reflect the existence of gene families involved in growth control.     

Localization of insulin-like growth factor genes to human chromosomes 11 and 12

The insulin-like growth factors IGF-I and IGF-II are required for growth and development. Both are single-chain proteins (of 70 and 67 amino acids respectively) derived from precursors by proteolytic processing. IGF-I may be particularly important in promoting normal stature and IGF-II may be a fetal growth hormone. The IGF proteins are probably synthesized by many normal tissues and by some tumours. The secretion of growth factors by tumours and tumour-derived cell lines suggests that they may act as autocrine regulators of cell proliferation. Because of the possible role of these proteins in growth disorders and cancer, and their sequence homology with insulin, we have determined their chromosomal localization. Using somatic cell hybrids and cloned cDNA probes for these proteins, we have assigned the genes for IGF-I and IGF-II to human chromosomes 12 and 11, respectively. We present evidence that the IGF-II gene is located on the short arm of chromosome 11 with a ras proto-oncogene and the insulin structural gene, and also suggest the existence of a fragment length polymorphism using the IGF-I probe.     

Insulin-like growth factor II precursor gene organization in relation to insulin gene family

The insulin gene family, comprised of insulin, relaxin, insulin-like growth factors I and II (IGF-I and IGF-II) and possibly the beta-subunit of 7S nerve growth factor, represents a group of structurally related polypeptides whose biological functions have diverged. The IGFs, or somatomedins, constitute a class of polypeptides that have a key role in pre-adolescent mammalian growth (see ref. 4 for review). IGF-I expression is regulated by growth hormone and mediates postnatal growth, while IGF-II appears to be induced by placental lactogen during prenatal development. The primary structures of both human IGFs have been determined and are closely related. A polypeptide highly homologous to human IGF-II is secreted by the rat liver cell line, BRL-3A. As this polypeptide, termed multiplication stimulating activity (MSA), differs from human IGF-II by only five amino acid residues, MSA probably represents the rat IGF-II protein. Using molecular cloning techniques, we have isolated cDNA and chromosomal genes coding for the MSA and human IGF-II precursors, respectively. Our data, presented here, indicate that both MSA and human IGF-II are synthesized initially as larger precursor molecules. The deduced preprohormones both have molecular weights (MWs) of 20,100 and contain C-terminal propeptides of 89 amino acid residues, which we have named E-peptides. The organization of the IGF-II precursor gene is discussed in relation to that of other insulin gene family members.     

荧光实时定量PCR检测尼罗罗非鱼GH、GHR、IGF-I基因方法的建立及初步应用

 为了准确分析尼罗罗非鱼生长激素（growth hormone , GH）、生长激素受体（growth hormone receptors, GHRs）和胰岛素样生长因子I （Insulin like growth factor-I,IGF I）在早期发育阶段的作用,实验设计了尼罗罗非鱼GH、GHR、IGF I基因的特异性引物,提 取垂体或肝脏总RNA并扩增出目的片段,将PCR产物克隆到pGEM-T Easy载体,经质粒PCR扩增、酶切和测序鉴定重组质粒,构建 标准曲线等,成功建立了GH、GHR、IGF-I基因荧光实时定量PCR检测方法。运用建立的荧光实时定量 PCR检测了尼罗罗非鱼GH 、GHR和IGF I基因表达的发育性变化。结果表明在早期发育阶段,尼罗罗非鱼GH 与 IGF-I,GHR1与 GHR2的mRNA表达存在一 定的互补关系;GH的表达与GHR1的表达呈显著正相关,提示GH与IGF-I,GHR1与GHR2在尼罗罗非鱼早期发育的不同阶段起主导 作用,且GH可能主要通过与GHR1的结合起作用。     

肥胖的风险与平板运动心电图诊断(综述)

通过文献资料法、实践观察法等研究方法研究了肥胖引起的合并症、肥胖患者在运动中存在的风险、以及肥胖的治疗和预防。研究结果发现,近年来肥胖的现象在全球越来越普遍,由于生活习惯等因素的改变,出现很大一部分超重或者肥胖的人群。这些人群可能出现冠心病、Ⅱ型糖尿病、胰岛素抵抗、高胰岛素血症、脂肪肝等各种合并症,并且在运动中存在潜在危险。平板运动心电图试验是诊断冠心病、评价心功能和运动耐力的简便有效的方法,通过试验可以诱发心律失常状况,或加重心血管疾病的某些症状,从而发现具有运动风险的人群,并对其运动负荷和持续时间提供指导。治疗和预防肥胖需要家庭、学校、工作场所、社区等多方面的支持。     

减量运动训练对急性肺栓塞患者康复状况的影响

研究减量运动训练对急性肺栓塞患者康复状况的影响,选择某大型综合医院的急性肺栓塞患者80例作为研究对象,随机将其划分成减量运动组和对照组,对照组在实验期间不进行任何形式的运动,减量运动组共进行6周的减量运动训练。结果减量运动组实验前后形态学指标之间的差异有统计学意义(P0.05);实验后减量运动组BMI、腰臀比和对照组相比差异有统计学意义(P0.05),腰围、臀围与对照组相比存在显著性差异(P0.01)。减量运动组血脂指标、血糖和胰岛素实验后与实验前相比,差异有统计学意义(P0.05),尿酸实验前后有显著性差异(P0.01);实验后减量运动组甘油三酯、胆固醇、低密度脂蛋白胆固醇、血糖和胰岛素与对照组相比差异有统计学意义(P0.05),高密度脂蛋白胆固醇、尿酸与对照组相比存在显著性差异(P0.01)。减量运动组实验后静脉血流速度明显高于实验前,差异具有显著性(P0.01);减量运动组实验后静脉血流速度明显高于对照组,差异具有显著性(P0.01)。减量运动组肺容量指标实验后与实验前相比,差异有统计学意义(P0.05);实验后减量运动组VC、IRV、TV与对照组相比差异有统计学意义(P0.05)。减量运动组FVC%实验后与实验前相比,差异有统计学意义(P0.05),MVV实验前后有显著差异(P0.01);实验后减量运动组FVC、MVV与对照组相比存在显著性差异(P0.01)。减量运动训练有助于急性肺栓塞患者的康复。     

运动、生长激素与衰老

就衰老与机体生长激素的关系、运动促进生长激素分泌的作用出发,结合过量外源性生长激素会导致的副作用,指出运动训练才是延缓衰老、改善老年人体能状况的科学、有效的方法。