C14]linoleic acid and [H3]cholesterol by gavage. Lymph was collected following cannulation of the lymph duct and radiolabelled chylomicrons were isolated by ultracentrifugation. The chylomicrons from each animal were injected into paired control and diabetic recipients. Lymph apolipoprotein (apo) B48, apo B100, and apo E were measured using sodium dodecyl sulfate–polyacrylamide gradient gel electrophoresis. Mean blood sugar of the diabetic donors and diabetic recipients were 19.7 ± 2.3 and 17.2 ± 3.2 mmol/L. Diabetic rabbits had significantly raised plasma triglyceride (10.8 ± 13.9 versus 0.8 ± 0.5 mmol/L, P < 0.02). There was a large increase in apo B48 in lymph chylomicrons in the diabetic donor animals (0.19 ± 0.10 versus 0.04 ± 0.02 mg/h, P < 0.01) and apo B100 (0.22 ± 0.15 versus 0.07 ± 0.07 mg/h, P < 0.05) and a reduction in apo E on the lymph chylomicron particle (0.27 ± 0.01 versus 0.62 ± 0.07 mg/mg apo B, P < 0.001). Diabetic recipients cleared both control and diabetic chylomicron triglyceride significantly more slowly than control recipients (P < 0.05). Clearance of control chylomicron cholesterol was delayed when injected into diabetic recipients compared to when these chylomicrons were injected into control recipients (P < 0.005). Clearance of diabetic chylomicron cholesterol was significantly slower when injected into control animals compared to control chylomicron injected into control animals (P < 0.02). In this animal model of atherosclerosis, we have demonstrated that diabetes leads to the production of an increased number of lipid and apo E–deficient chylomicron particles. Chylomicron particles from the control animals were cleared more slowly by the diabetic recipient (both triglyceride and cholesterol). The chylomicron particles obtained from the diabetic animals were cleared even more slowly when injected into the diabetic recipient. Although there was an initial delay in clearance of chylomicron triglyceride from the diabetic particle when injected into the control animals, the clearance over the first 15 minutes was not significantly different when compared to the control chylomicron injected into the control animal. On the other hand, the cholesterol clearance was significantly delayed. Thus, diabetes resulted in the production of an increased number of lipid- and apo E–deficient chylomicron particles. These alterations account, in part, for the delay in clearance of these particles."> 有缺陷的乳糜微粒合成作为糖尿病的原因推迟粒子间隙? - raybet雷竞app,雷竞技官网下载,雷电竞下载苹果

糖尿病研究期刊》的研究

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体积 3 |文章的ID 249798年 | https://doi.org/10.1080/15604280214277

凯瑟琳·菲利普斯,克莱尔·马迪根达芙妮•欧文斯,杰拉尔德·h·Tomkin帕特里克·柯林斯, ”有缺陷的乳糜微粒合成作为糖尿病的原因推迟粒子间隙?”,糖尿病研究期刊》的研究, 卷。3, 文章的ID249798年, 8 页面, 2002年。 https://doi.org/10.1080/15604280214277

有缺陷的乳糜微粒合成作为糖尿病的原因推迟粒子间隙?

凯瑟琳•菲利普斯,¹ 克莱尔·马迪根,¹ 达芙妮•欧文斯,¹ 帕特里克•柯林斯,² 和杰拉尔德·h·Tomkin^1,3,4

¹临床医学、爱尔兰都柏林三一学院

²生物化学、皇家外科学院在爱尔兰,都柏林,爱尔兰

³内分泌和糖尿病,阿德莱德/米斯郡医院,都柏林,爱尔兰

⁴1,费茨威廉广场,爱尔兰都柏林2

收到了 2001年11月20日

接受 2002年1月24日

文摘

乳糜微粒代谢异常在糖尿病和乳糜微粒粒子可能在动脉粥样硬化中发挥非常重要的作用。本研究的目的是检查糖尿病对新陈代谢的影响之内在cholesterol-fed四氧嘧啶糖尿病和非糖尿病的兔子。控制糖尿病兔子和5只兔子有( C 14 亚油酸和( H 3 强饲法)胆固醇。淋巴收集后中空淋巴导管和放射性标记之内被超速离心法分离。乳糜微粒从每个动物注入配对控制和糖尿病人。淋巴阿朴脂蛋白(apo) B48、apo B100和apo E测定使用钠十二烷基sulfate-polyacrylamide梯度凝胶电泳。意味着糖尿病捐助者和糖尿病人的血糖为19.7±2.3,17.2±3.2更易/ L。糖尿病兔明显提高血浆甘油三酯(10.8±13.9和0.8±0.5更易与L,P< 0.02)。有了很大的提升在淋巴apo B48乳糜微粒在糖尿病供体动物(0.19±0.10和0.04±0.02毫克/ h,P< 0.01)和apo B100(0.22±0.15和0.07±0.07毫克/ h,P< 0.05)和减少apo E淋巴乳糜微粒粒子(0.27±0.01和0.62±0.07毫克/毫克apo B,P< 0.001)。糖尿病患者接受了两个控制和糖尿病乳糜微粒比控制收件人(甘油三酯明显更慢P< 0.05)。间隙控制乳糜微粒胆固醇被推迟,当注入乳糜微粒相比,糖尿病人当这些被注入控制收件人(P< 0.005)。间隙的糖尿病乳糜微粒胆固醇明显慢时注入控制动物相比,控制乳糜微粒注入控制动物(P< 0.02)。在动脉粥样硬化动物模型,我们表明,糖尿病导致的生产数量的增加脂质和apo E-deficient乳糜微粒颗粒。乳糜微粒颗粒从控制糖尿病动物被清除更慢的收件人(甘油三酯和胆固醇)。乳糜微粒颗粒从糖尿病动物获得了更缓慢注入到糖尿病收件人。尽管有乳糜微粒的初始延迟清除甘油三酯的糖尿病粒子注入控制动物的时候,第一个15分钟的间隙控制乳糜微粒相比,没有明显不同注入控制动物。另一方面,胆固醇间隙明显延迟。因此,糖尿病导致的生产数量的增加脂质-和apo E-deficient乳糜微粒颗粒。这些改变帐户,在某种程度上,这些粒子的延误清关。

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