微量元素铬与运动的关系

铬是动物机体必需微量元素之一,在人体中代谢中也起着重要的作用,它可以作为葡萄糖耐受因子的组成成分,协助胰岛素发挥生理功能。它可促进胰岛素的生物学功能,同时控制着氛基酸、糖和脂代谢全过程,缺铬能影响糖耐量和引起血脂代谢紊乱,引起疾病。运动可导致机体对铬需求的增加,铬补充对运动员肌肉力量、瘦体重可产生较好影响。本文主要综述了铬在人体内的存在与代谢,生物学作用,以及其与糖代谢的关系。     

运动对GLUT4影响的研究进展

葡萄糖跨膜转运是机体利用葡萄糖的首要步骤。葡萄糖载体(GLUT)是细胞膜上介导葡萄糖跨膜转运的蛋白质,它们对机体的葡萄糖利用有重要意义。运动可有效增加外周组织(主要为骨骼肌和脂肪组织)细胞膜葡萄糖载体4(GLUT4)的数量,使细胞内GLUT4的囊泡数量增多,GLUT4mRNA的表达增强,有效地加快血糖的转移、吸收和利用,解除外周组织胰岛素抵抗,调节血糖平衡,对糖尿病人的治疗有积极的作用和意义。     

运动对胰岛功能影响的研究进展

2型糖尿病的病理生理改变主要是从胰岛素抵抗为主伴随胰岛素分泌不足，转变到胰岛素分泌不足为主伴胰岛素抵抗，影响胰岛功能正常发挥，进而导致慢性高血糖的代谢疾病。科学合理的运动可以恢复胰岛细胞的功能，增加胰岛素敏感性，减轻胰岛素的抵抗现象、促进机体对糖的利用，从而改善2型糖尿病患者胰岛功能和糖代谢的调节作用。因此，养成良好的运动习惯对糖尿病的预防具有积极的促进作用。     

运动对RBP4 诱导的胰岛素抵抗大鼠骨骼肌PI3- K表达的影响

目的：研究运动对RBP4 诱导的胰岛素抵抗大鼠骨骼肌PI3- K表达的影响。方法：8 周龄雄性SD 大鼠给予重组RBP43μgg- 1 体重腹腔注 射，12 小时注射一次，持续注射3 周。设RBP4+ 运动组（RE）、RBP4 安静组（RR）和正常安静对照组（C），RE 组予3 周无负重游泳训练，60 min/ 天.ELISA、液闪计、免疫组化和免疫印迹法分别检测血清RBP4，胰岛素抵抗指数HOMA- IR、葡萄糖摄取率和骨骼肌PI3- K表达。结果：RBP4 注射组血清RBP4 和HOMA- IR 显著高于未注射RBP4 的正常安静对照组，葡萄糖摄取率显著低于正常安静对照组；RE 组血清RBP4 和HOMA- IR 显 著低于RR 组，葡萄糖摄取率显著高于RR 组。RE 组骨骼肌细胞PI3- K蛋白表达显著高于RR 组。结论：游泳运动能够增加RBP4 诱导的胰岛素 抵抗大鼠骨骼肌PI3- K表达，促进葡萄糖摄取，改善胰岛素抵抗。     

逃离衰老的定时炸弹

在人的血液中，有一种由胰腺器官中的B细胞制造出来的胰岛素，食物在人体内被转化成葡萄糖后，要借由胰岛素将它从血液传送到细胞内，以转变为能量。所以，正常水平的胰岛素对身体健康十分关键。但是，当人进入35岁以后，尤其是随着年龄的增加，一天天开始发胖的情况下，由于血液中含有胰岛素的抗体，会使胰岛素的效力减弱。也有人由于精神因素引起内分泌疾病，导致机体组织对胰岛素有抵抗，自身胰岛素敏感性下降，不能分泌足够的胰岛素，这意味着细胞阻止了胰岛素把糖分转移到细胞中转化成能量的正常工作。为了保持血液中糖分水平的正常，…     

运动对RBP4诱导的胰岛素抵抗鼠骨骼肌PTP1B表达的影响

目的研究运动对RBP4诱导的胰岛素抵抗大鼠骨骼肌PTP1B表达的影响,探讨运动影响RBP4诱导的胰岛素抵抗机制。方法 8周龄雄性SD大鼠给予重组RBP4腹腔注射,建立胰岛素抵抗鼠模型。设RBP4+运动组(RE)、RBP4+安静组(RQ)和正常安静对照组(C),RE组予3周游泳训练。ELISA、液闪计、免疫组化法、免疫印记法和RT-PCR法分别检测血清RBP4,胰岛素敏感指数QUICK I、葡萄糖摄取率和骨骼肌PTP1B、GLUT4 mRNA表达。结果 RE和RQ组血清RBP4和PTP1B表达显著高于C组,葡萄糖摄取率、QUICK I和GLUT4 mRNA表达显著低于C组;3周游泳训练后,RE组血清RBP4和骨骼肌PTP1B表达显著低于RQ组,葡萄糖摄取率、QUICK I和GLUT4 mRNA表达显著高于RQ组。结论 3周游泳运动能够显著降低RBP4诱导的胰岛素抵抗大鼠骨骼肌PTP1B表达,增加GLUT4 mRNA表达,促进葡萄糖摄取,改善胰岛素抵抗。     

运动对胰岛功能影响的研究进展

2型糖尿病的病理生理改变主要是从胰岛素抵抗为主伴随胰岛素分泌不足,转变到胰岛素分泌不足为主伴胰岛素抵抗,影响胰岛功能正常发挥,进而导致慢性高血糖的代谢疾病.科学合理的运动可以恢复胰岛细胞的功能,增加胰岛素敏感性,减轻胰岛素的抵抗现象、促进机体对糖的利用,从而改善2型糖尿病患者胰岛功能和糖代谢的调节作用.因此,养成良好的运动习惯对糖尿病的预防具有积极的促进作用.     

运动调节脂肪细胞因子的研究进展

靶组织胰岛素敏感性降低导致的胰岛素抵抗是许多疾病的发病基础,脂肪组织作为胰岛素主要靶器官是机体最大的储能器官,它的内分泌功能是调节能量平衡的重要因子,早已证实,脂肪与胰岛素抵抗发病有密切的相关性,其通过内分泌、自分泌、旁分泌产生瘦素、肿瘤坏死因子α、脂联素、抵抗素、白介素-6等细胞因子和激素调节血糖动态平衡,脂肪细胞因子代谢异常是引起胰岛素抵抗的重要原因之一。通过持续有氧运动、间歇有氧运动、抗阻力运动等多种方式对脂肪细胞因子表达的改善可促进胰岛素相关信号转导途径MAPK、PI3K中的关键蛋白表达进而促进胰岛素信号转导,实现改善胰岛素抵抗。     

胰岛素与运动能力的关系

胰岛素是一种作用较强的代谢调节激素,全面促进机体的合成代谢,临床上常用来治疗糖尿病患者,维持其血糖的稳定。胰岛素对运动员的成绩影响,主要体现在胰岛素可以促进葡萄糖的分解代谢合成肌糖元,使肌糖原储备增加、延缓运动性疲劳,从而提高运动成绩。本文通过文献资料法,对胰岛素的生化功能及其对运动能力的影响进行综合阐述。     

AMPK与2型糖尿病的关系及其在运动介导下的研究

腺苷酸活化蛋白激酶（AMPK）是一种重要的蛋白激酶，其主要作用是协调代谢和能量平衡。AMPK被激活后在增加骨骼肌对葡萄糖摄取、增强胰岛素敏感性方面发挥重要作用。由于在调节糖代谢方面的作用，AMPK为治疗胰岛素抵抗和2型糖尿病提供了新的药理靶点。     

AS160与TBC1D1:胰岛素和运动/骨骼肌收缩诱导葡萄糖转运的汇聚点

运动和胰岛素是诱导骨骼肌葡萄糖转运的两种重要生理因素，两者均能通过不同的信号转导通路诱导GLUT4从细胞内转位到细胞膜表面，从而调控骨骼肌的葡萄糖转运。研究表明，TBC1家族结构域家族成员蛋白激酶B蛋白底物160KDa（AS160/TBC1D4）和TBC1D1这两种同源蛋白均可在运动或胰岛素诱导下发生磷酸化，两者可能是运动和胰岛素调控骨骼肌葡萄糖转运信号通路的关键汇聚点。综述AS160与TBC1D1在胰岛素诱导骨骼肌葡萄糖转运中的不同作用以及运动/骨骼肌收缩对其的影响及其机制，以期深入了解运动如何改善胰岛素敏感性、为更科学的运动处方及其他干预措施的研发提供有价值的理论支持。     

Effect of a prolonged altitude expedition on glucose tolerance and abdominal fatness

In the present study, we investigated the effect of a long-term mountain expedition on glucose tolerance and insulin action. Twelve registered mountaineers ages 31 years (SD = 1.1) participated in a 25-day expedition at a 2,200-3,800-m altitude with an average duration of 8 hr per day. Arterial oxygen saturation (SaO2) was substantially reduced during hiking. Glucose tolerance and insulin responses were measured prior to and twice during the expedition period. Maximal oxygen consumption increased from 43.0 +/- 2.7 to 49.1 +/- 2.2 mL/kg/min. Percentage of body fat decreased from 19.4 +/- 6.8% to 16.9 +/- 5.9%. The area under the curves for insulin and glucose during the oral glucose tolerance test were also reduced in Days 3 and 25. The present study demonstrated that altitude hiking activity is an effective lifestyle intervention to improve insulin action.     

Effect of a Prolonged Altitude Expedition on Glucose Tolerance and Abdominal Fatness

In the present study, we investigated the effect of a long-term mountain expedition on glucose tolerance and insulin action. Twelve registered mountaineers ages 31 years (SD = 1.1) participated in a 25-day expedition at a 2,200-3,800-m altitude with an average duration of 8 hr per day. Arterial oxygen saturation (SaO2) was substantially reduced during hiking. Glucose tolerance and insulin responses were measured prior to and twice during the expedition period. Maximal oxygen consumption increased from 43.0 ± 2.7 to 49.1 ± 2.2 mL/kg/min. Percentage of body fat decreased from 19.4 ± 6.8% to 16.9 ± 5.9%. The area under the curves for insulin and glucose during the oral glucose tolerance test were also reduced in Days 3 and 25. The present study demonstrated that altitude hiking activity is an effective lifestyle intervention to improve insulin action.     

健步走对糖耐量减低患者脂联素和内皮依赖性血管舒张功能的影响

目的:探讨健步走运动锻炼对糖耐量减低(IGT)患者血清脂联素、内皮依赖性血管舒张功能的影响。方法:对41名糖耐量减低患者随机分为健步走组20名、对照组21名,受试者采取24周运动处方的锻炼。运动干预前、后测定身体成分、脂联素(Adiponectin)、空腹血糖、餐后2h血糖和空腹胰岛素,计算胰岛素抵抗指数(HOMA-IR),并采用高分辨血管外超声法检测肱动脉血流介导的内皮依赖性血管舒张功能(EDD)和硝酸甘油介导的内皮非依赖性血管舒张功能(EID)。结果:1)24周运动干预后,健步走组体脂%、腰围、腰臀围比、餐后2h血糖、空腹胰岛素、HOMA-IR均明显下降,血脂联素水平升高,内皮依赖性血管舒张功能明显改善;2)脂联素变化量的多元逐步回归分析显示出2个预测变量:体脂%、腰围的变化量。结论:对IGT患者进行健步走运动干预可升高血清脂联素水平,改善内皮依赖性血管舒张功能。     

Insulin sensitivity derived from oral glucose tolerance testing in athletes: Disagreement between available indices

The aims of the present study were to determine whether available “fasting” and oral glucose tolerance test-derived insulin sensitivity indices could effectively discriminate between individuals with higher than normal insulin sensitivity, and whether they would all provide similar information in clinical practice. Sprint runners (n = 8), endurance runners (n = 8) and sedentary controls (n = 7) received a 75-g oral glucose tolerance test. All participants were healthy lean males, aged 21?–?29 years. Besides glucose and insulin responses, a total of nine such indices were computed. Fasting as well as post-load glucose concentrations were similar in the three groups, while basal plasma insulin and the insulinaemic response to glucose were both higher in untrained individuals (at P?<?0.05 and P?<?0.02, respectively). There were no differences between endurance and sprint runners. The results for insulin sensitivity, however, were quite variable: three indices showed that both groups of athletes were more insulin-sensitive than controls; three indicated that this was the case for endurance runners only; one indicated that this was the case for sprint runners only; and two showed that sprint runners were more insulin-sensitive than either sedentary individuals or endurance runners (all differences were significant at P?<?0.05). Controlling for total body weight or lean mass did not effectively resolve this disagreement. Apparently, the various insulin sensitivity indices examined provided different quantitative and qualitative information, despite insulin action being greater in both groups of athletes relative to controls, as reflected by their similar glucose tolerance with lower insulin concentrations. We suggest, therefore, that the use and interpretation of such indices among physically active individuals be made with caution.     

Insulin sensitivity derived from oral glucose tolerance testing in athletes: disagreement between available indices

The aims of the present study were to determine whether available "fasting" and oral glucose tolerance test-derived insulin sensitivity indices could effectively discriminate between individuals with higher than normal insulin sensitivity, and whether they would all provide similar information in clinical practice. Sprint runners (n = 8), endurance runners (n = 8) and sedentary controls (n = 7) received a 75-g oral glucose tolerance test. All participants were healthy lean males, aged 21-29 years. Besides glucose and insulin responses, a total of nine such indices were computed. Fasting as well as post-load glucose concentrations were similar in the three groups, while basal plasma insulin and the insulinaemic response to glucose were both higher in untrained individuals (at P < 0.05 and P < 0.02, respectively). There were no differences between endurance and sprint runners. The results for insulin sensitivity, however, were quite variable: three indices showed that both groups of athletes were more insulin-sensitive than controls; three indicated that this was the case for endurance runners only; one indicated that this was the case for sprint runners only; and two showed that sprint runners were more insulin-sensitive than either sedentary individuals or endurance runners (all differences were significant at P < 0.05). Controlling for total body weight or lean mass did not effectively resolve this disagreement. Apparently, the various insulin sensitivity indices examined provided different quantitative and qualitative information, despite insulin action being greater in both groups of athletes relative to controls, as reflected by their similar glucose tolerance with lower insulin concentrations. We suggest, therefore, that the use and interpretation of such indices among physically active individuals be made with caution.     

磷酯酰肌醇3激酶在骨骼肌中的调节以及运动对它的影响

在骨骼肌中磷酯酰肌醇3激酶(PI3K)以异二聚体形态存在.它以及它下游的靶目标和胰岛素受体底物(IRS1,2)一起在胰岛素信号转导通路中发挥重要作用,并参与了胰岛素刺激的葡萄糖转运和GLUT-4转移;不同强度运动以及运动时间对骨骼肌中PI3K有着不同的作用,这也和胰岛素的调节有关.     

A single bout of high-intensity interval exercise and work-matched moderate-intensity exercise has minimal effect on glucose tolerance and insulin sensitivity in 7- to 10-year-old boys

The purpose of this study was to assess the acute effect of high-intensity interval exercise (HIIE) and moderate-intensity exercise (MIE) on glucose tolerance, insulin sensitivity and fat oxidation in young boys. Eleven boys (8.8 ± 0.8 y) completed three conditions: 1) HIIE; 2) work-matched MIE; and 3) rest (CON) followed by an oral glucose tolerance test (OGTT) to determine glucose tolerance and insulin sensitivity (Cederholm index). Fat oxidation was measured following the OGTT using indirect calorimetry. There was no effect for condition on plasma [glucose] and [insulin] area under the curve (AUC) responses following the OGTT (P > 0.09). However, there was a “trend” for a condition effect for insulin sensitivity with a small increase after HIIE (P = 0.04, ES = 0.28, 9.7%) and MIE (P = 0.07, ES = 0.21, 6.5%) compared to CON. There was an increase in fat oxidation AUC following HIIE (P = 0.008, ES = 0.79, 38.9%) compared to CON, but with no differences between MIE and CON and HIIE and MIE (P > 0.13). In conclusion, 7- to 10-year-old boys may have limited scope to improve insulin sensitivity and glucose tolerance after a single bout of HIIE and MIE. However, fat oxidation is augmented after HIIE but not MIE.