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在应用实时荧光定量PCR法观察胰岛素(In)、胰高血糖素(GLN)、神经肽(NPY)对体外培养新生犊牛肝细胞硬脂酰CoA去饱和酶(Stearoyl CoA desaturase,SCD) mRNA丰度的影响.结果显示,随着培养液中In含量的升高,肝细胞中的SCD mRNA表达逐渐升高(P＜0.05),呈现明显的剂量依赖促进效应;随着培养液中GLN含量的升高,肝细胞SCD mRNA丰度表达逐渐减弱,高血糖素处理组SCD mRNA表达均极显著低于对照组(P＜0.01);而随着NPY质量浓度在0～1 000 ng/L之间逐渐上升,肝细胞SCDmRNA的表达水平不断升高,各处理组显著高于对照组,除50 ng/L处理组和500 ng/L处理组之间差异不显著外,其他处理组之间差异显著(P＜0.05).结果表明,胰岛素和神经肽Y促进SCD mRNA表达,胰高血糖素抑制SCD mRNA表达. 相似文献
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铜对体外仔猪软骨细胞增殖和自分泌IGF-Ⅰ、IGFBP3的影响 总被引：4，自引：0，他引：4
体外分离、培养仔猪关节软骨细胞,然后在细胞培养液中分别添加0、7.8、15.6、31.2、62.5μmol/L铜.结果表明,软骨细胞在4种浓度的铜中可存活并增殖,而且能增加胰岛素样生长因子(IGF-Ⅰ)、胰岛素样生长因子结合蛋白(IGFBP3)的分泌量.但随铜浓度的增加,其存活率、增殖率、3H-TdR掺入率及IGF-Ⅰ、IGFBP3的分泌量有明显的差异.且以培养液中添加31.2μmol/L铜对软骨细胞的增殖作用最强,增殖率、3H-TdR掺入数、IGF-Ⅰ、IGFBP3的分泌量显著高于对照组(P＜0.01).表明31.2μmol/L铜浓度是促进体外软骨细胞增殖和自分泌IGF-Ⅰ、IGFBP3的最适浓度. 相似文献
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《中国兽医学报》2016,(3):508-512
旨在探讨非酯化脂肪酸(nonestesterified fatty acids,NEFAs)对体外原代培养犊牛肝细胞胰岛素信号通路的影响及SIRT1在其中的调控作用。选择培养48h的原代犊牛肝细胞,添加不同浓度的NEFAs(0、0.6、1.2、1.8mmol/L),继续培养12h,胰岛素处理组在收样前用100nmol/L胰岛素处理30min,每个浓度3个重复。另外选取已培养48h的细胞,用SIRT1抑制剂Nicotinamide(10mmol/L)处理12h,胰岛素处理组在收样前用100 mmol/L胰岛素处理30min。运用免疫印迹Western blot方法,检测NEFAs和Nicotinamide对肝细胞胰岛素信号通路关键蛋白IR和Akt的磷酸化水平及SIRT1蛋白表达水平的影响。结果显示,与对照组相比,1.2、1.8 mmol/L NEFAs组胰岛素刺激的IR磷酸化水平显著降低(P0.01),而Akt的磷酸化程度在NEFAs浓度为0.6 mmol/L时即显著降低(P0.01),同时,SIRT1的蛋白表达水平在NEFAs为1.2、1.8mmol/L显著降低(P0.01);添加SIRT1抑制剂显著降低SIRT1的蛋白表达水平(P0.01),同时胰岛素刺激的Akt磷酸化水平也显著降低(P0.01)。结果表明,高浓度的NEFAs可以损伤体外原代培养肝细胞的胰岛素信号通路,SIRT1在NEFAs损伤的胰岛素信号通路中发挥重要作用。 相似文献
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乐果引起大鼠肝细胞凋亡的机理 总被引：2，自引：0，他引：2
通过给大鼠肝细胞培养液中加入乐果(0、3、10、30、100、300μmol/L),染毒122、4 h后,Annexin V/PI双染法检测肝细胞凋亡率;分别用Fluo-2/AM、双氢-乙酰乙酸二氯荧光黄(DCFH-DA)和罗丹名123检测细胞内Ca2+浓度、活性氧(ROS)和线粒体膜电位(Δψm)变化,并在扫描电镜和荧光显微镜下观察凋亡细胞情况,探讨乐果对大鼠肝细胞凋亡的影响。结果显示,肝细胞染毒12、24 h后,出现了明显的细胞凋亡的形态学变化,细胞凋亡率明显升高,除3μmol/L组外,与对照组相比差异显著(P0.05或P0.01),且呈时间-剂量效应。3μmol/L组细胞内Ca2+浓度极显著高于对照组(P0.01),之后随染毒剂量的增加,细胞内Ca2+浓度逐渐下降;细胞内ROS水平在3~100μmol/L随染毒剂量的增大和染毒时间的延长而升高,而在300μmol/L组略有下降,除3μmol/L组外,与对照组相比均差异极显著(P0.01);Δψm除24 h 300μmol/L组外均出现持续下降。结果表明,低剂量乐果染毒可诱导肝细胞发生凋亡,细胞内Ca2+、ROS和Δψm可能参与了这一过程。 相似文献
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在原代单层培养的新生犊牛肝细胞培养液中分别加入不同浓度丙酸钠、丙酮酸钠、胰岛素、胰高血糖素和瘦蛋白，培养12h后，应用半定量RT-PCR方法检测体外培养的肝细胞PEPCK—C mRNA的丰度。结果显示，随着丙酸钠、丙酮酸钠浓度的升高，肝细胞PEPCK-C mRNA的丰度均先升高后下降（P〈0．01）；随胰岛素、胰高血糖素和瘦蛋白浓度的升高，肝细胞PEPCK-C mRNA的丰度分别剂量依赖性地降低、升高（P〈0．01）和无显著变化。表明，丙酸钠、丙酮酸钠能通过上调体外培养的新生犊牛肝细胞PEPCK—C mRNA的表达而促进肝糖异生代谢，但上调作用是有限的；胰岛素能通过下调体外培养的新生犊牛肝细胞PEPCK—C mRNA的表达而抑制肝糖异生代谢，且下调作用呈剂量依赖性；胰高血糖素与胰岛素作用刚好相反；瘦蛋白未起直接的调节作用。 相似文献
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在成功构建牛肝细胞培养模型和PC基因DNA竞争模板的基础上，采用竞争RT—PCR方法检测了丙酸钠和丙酮酸钠对体外培养新生牛单层肝细胞PC基因mRNA丰度的影响。结果，随着丙酸钠浓度的升高，PC基因mRNA水平呈上升趋势，PC基因mRNA对丙酸钠的耐受范围较广；随着丙酮酸钠浓度的升高PC基因mRNA水平呈先上升后下降的趋势。结果表明，肝细胞内PC基因mRNA的表达水平受丙酮酸钠浓度的调控，在一定范围内丙酮酸钠对PC基因mRNA的转录具有促进作用，而浓度过高时则起抑制作用。 相似文献
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为了阐明神经内分泌因子在奶牛肝脂蛋白组装与转运过程中的调控作用,通过向体外培养的新生犊牛肝细胞添加胰岛素、胰高血糖素和瘦蛋白,采用内对照RT-PCR方法检测神经内分泌因子对体外培养新生犊牛肝细胞微粒体甘油三酯转运蛋白(MTP)mRNA丰度的影响。结果显示,随着细胞培养液中胰岛素和胰高血糖素浓度升高,MTP mRNA的丰度呈现剂量依赖性下降(P<0.01);随着瘦蛋白浓度的增加,MTP mRNA的丰度先升高后降低(P<0.01或P<0.05)。这表明胰岛素和胰高血糖素对肝细胞MTP mRNA表达具有抑制作用,呈现剂量依赖性;瘦蛋白对肝细胞MTP mRNA表达具有低剂量促进而高剂量抑制的双重作用,且均呈现剂量依赖性。 相似文献
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铜导致肉鸡肝细胞游离钙的超载 总被引：1，自引：1，他引：0
选用硫酸铜作为试验铜源,向即时分离的肉鸡肝细胞悬液中加入不同剂量的铜(铜终浓度分别为:0,5,10,20,30μmol/L),孵育不同时间(5,10,15,20,30 min)后观察肝细胞内游离钙浓度的变化.结果显示:高剂量的铜可破坏细胞内游离钙稳态.钙内流造成细胞内钙超载,30μmol/L铜刺激组的[Ca2+]i显著高于对照组(P<0.05).肝细胞在10 μmol/L Cu2+环境中孵育不同时间后显示,时间越长.细胞内钙浓度越高;此结果表明,10μmol/L铜能诱导细胞内游离钙的超载,并具有浓度依赖性和时间依赖性,暗示铜对体细胞的毒害作用可能是通过改变细胞内游离钙浓度来实现. 相似文献
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镉对大鼠原代肝细胞的毒性损伤 总被引：3，自引：0，他引：3
用两步灌流法获得大鼠肝细胞,肝细胞暴露于浓度为2.5、5、10μmol/L的醋酸镉24 h.测定了细胞活力、培养上清液中乳酸脱氢酶(LDH)、天冬氨酸转氨酶(AST)和丙氨酸转氨酶(ALT)活性及细胞内谷胱甘肽过氧化物酶(GSH-PX)活性、还原型谷胱甘肽(GSH)和丙二醛(MDA)含量的变化.结果表明,细胞相对存活率显著下降(P<0.01),LDH、AST和ALT的释放量增加,5μmol/L和10 μmol/L剂量组与对照组相比差异均显著(P<0.01),细胞内GSH-PX活性降低,各剂量染毒组与对照组相比,差异均极显著(P<0.01);细胞内GSH含量升高,5 μmol/L和10μmol/L剂量组与对照组差异均显著(P<0.05),细胞内MDA含量升高,10μmol/L剂量组与对照组相比差异显著(P<0.05).表明镉可致肝细胞损伤,并且氧化应激起了重要作用. 相似文献
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为了研究维生素C对铜孵育的肉鸡原代肝细胞周期及细胞膜电位的影响,试验将全量换液24 h后的原代肝细胞分为正常对照组(Ⅰ组)和10μmol/L Cu2+(Ⅱ组)、30μmol/L Cu2+(Ⅲ组)、50μmol/L Cu2+(Ⅳ组)、50μmol/L维生素C+50μmol/L Cu2+(Ⅴ组)刺激组,于体外刺激后48小时用流式细胞仪测定各组的细胞周期及细胞膜电位。结果表明:30μmol/L和50μmol/L Cu2+能明显引起静止期肝细胞数增多,增殖期肝细胞数减少,细胞膜电位下降(P<0.05),10μmol/L Cu2+组没有出现明显变化。说明维生素C可显著抑制50μmol/L Cu2+引起的变化,对细胞具有保护作用。 相似文献
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Abnormalities of insulin metabolism include hyperinsulinaemia and insulin resistance, and these problems are collectively referred to as insulin dysregulation in this review. Insulin dysregulation is a key component of equine metabolic syndrome: a collection of endocrine and metabolic abnormalities associated with the development of laminitis in horses, ponies and donkeys. Insulin dysregulation can also accompany prematurity and systemic illness in foals. Causes of insulin resistance are discussed, including pathological conditions of obesity, systemic inflammation and pituitary pars intermedia dysfunction, as well as the physiological responses to stress and pregnancy. Most of the discussion of insulin dysregulation to date has focused on insulin resistance, but there is increasing interest in hyperinsulinaemia itself and insulin responses to feeding. An oral sugar test or in‐feed oral glucose tolerance test can be performed to assess insulin responses to dietary carbohydrates, and these tests are now recommended for use in clinical practice. Incretin hormones are likely to play an important role in postprandial hyperinsulinaemia and are the subject of current research. Insulin resistance exacerbates hyperinsulinaemia, and insulin sensitivity can be measured by performing a combined glucose‐insulin test or i.v. insulin tolerance test. In both of these tests, exogenous insulin is administered and the rate of glucose uptake into tissues measured. Diagnosis and management of hyperinsulinaemia is recommended to reduce the risk of laminitis. The term insulin dysregulation is introduced here to refer collectively to excessive insulin responses to sugars, fasting hyperinsulinaemia and insulin resistance, which are all components of equine metabolic syndrome. 相似文献
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Blood Glucose and Insulin Concentrations after Octreotide Administration in Horses With Insulin Dysregulation 
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下载免费PDF全文 N. Frank P. Hermida A. Sanchez‐Londoño R. Singh C.M. Gradil C.K. Uricchio 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2017,31(4):1188-1192
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C. Gilor T.K. Ridge K.J. Attermeier T.K. Graves 《Journal of veterinary internal medicine / American College of Veterinary Internal Medicine》2010,24(4):870-874
Background: Insulin detemir and insulin glargine are synthetic long‐acting insulin analogs. In people, insulin glargine is longer acting and has a relatively flat time‐action profile, while insulin detemir has significantly less within‐subject variability. Insulin detemir is also associated with less undesired weight gain and decreased frequency of hypoglycemic events. Objectives: To compare the pharmacodynamics of insulin detemir and insulin glargine in healthy cats. Animals: Ten young, healthy, neutered, purpose‐bred cats. Methods: Randomized, cross‐over design. Pharmacodynamics of insulin detemir and insulin glargine were determined by the isoglycemic clamp method after a 0.5 U/kg SC injection. Results: The only significant difference in the pharmacodynamics of insulin detemir and insulin glargine was onset of action (1.8 ± 0.8 and 1.3 ± 0.5 hours for insulin detemir and insulin glargine, respectively, P= .03). End of action of insulin detemir was reached at 13.5 ± 3.5 hours and for insulin glargine at 11.3 ± 4.5 hours (P= .18). Time‐to‐peak action of insulin detemir was reached at 6.9 ± 3.1 hours and for insulin glargine at 5.3 ± 3.8 hours (P= .7). The time‐action curves of both insulin analogs varied between relatively flat curves in some cats and peaked curves in others. Conclusion and Clinical Importance: Insulin detemir and insulin glargine have shorter durations of action than in people when assessed by the clamp method, but in some cats these insulin analogs could be useful as once‐a‐day drugs. Peak effects of both insulin analogs are pronounced in some cats. 相似文献
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Sarah L Ralston 《Veterinary Clinics of North America: Equine Practice》2002,18(2):295-304, vii
Abnormally high or low blood glucose and insulin concentrations after standardized glucose tolerance tests can reflect disorders such as pituitary dysfunction, polysaccharide storage myopathies, and other clinical disorders. Glucose and insulin responses, however, are modified by the diet to which the animal has adapted, time since it was last fed, and what it was fed. Body fat (obesity), fitness level, physiologic status, and stress also alter glucose and insulin metabolism. Therefore, it is important to consider these factors when evaluating glucose and insulin tests, especially if only one sample it taken. This article describes the factors affecting glucose and insulin metabolism in horses and how they might influence the interpretation of standardized tests of glucose tolerance. 相似文献
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In the horse, resting insulin concentration (INS), the glucose-to-insulin ratio (G:I), and the reciprocal of the square root of insulin (RISQI = 1/√INS) are commonly used to estimate insulin sensitivity, whereas the modified insulin-to-glucose ratio (MIRG = [800 – 0.30 × (INS -50)2]/(GLU – 30) is used to estimate pancreatic beta-cell responsiveness. Because no estimates of their within-horse variability and repeatability have been reported, the objective of this study was to evaluate the within-horse variation of these estimates. Resting blood samples were obtained from six healthy equids (three geldings, two mares; mean ± SD body weight, 525.0 ± 43.36 kg; mean age, 9.8 ± 8.2 years; and one pony gelding: 293 kg; 12 years) on three consecutive days in week 1 and again in week 2. Samples were collected at 12:00 noon, approximately 6 hours postprandially. Serum insulin and plasma glucose (GLU) concentrations were analyzed and used to calculate G:I, RISQI, and MIRG, as well as the insulin to glucose ratio (I:G). The coefficient of variation was used to determine within-horse variation, and repeatability was determined using the repeatability coefficient (RC; measurements from a single horse should differ less than the RC for 95% of the pairs). The mean coefficients of variation (CVs) for resting GLU, INS, G:I, I:G, MIRG, and RISQI were 5.5%, 33.7%, 36.0%, 31.6%, 22.3%, and 18.6%, respectively. All variables had values that differed more than the RC in at least one horse. These data suggest that care should be taken when interpreting insulin sensitivity estimates from a single blood sample. 相似文献
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Laminitis is a devastating disease of horses that usually arises as a consequence of major systemic disease or endocrine disturbances. Research has been confounded by apparently disparate results and theories on pathogenesis. Models of laminitis have greatly advanced our understanding of the disease, yet have mostly involved perturbations of the gastrointestinal tract or inflammatory models. A major trend in research on laminitis in the past few years has been the increasing interest in endocrine dysfunction resulting in laminitis. A new model of laminitis associated with hyperinsulinemia has recently been discovered and the central role of high insulin in triggering endocrinopathic laminitis highlighted. This review discusses the pathophysiology of insulin resistance and hyperinsulinemia in horses and possible mechanisms of insulin-induced laminitis. 相似文献