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甲状旁腺激素相关蛋白对肝脏胰岛素样生长因子-1生成的影响。

The influence of parathyroid hormone-related protein on hepatic IGF-1 production.

作者信息

Coxam V, Davicco M J, Durand D, Bauchart D, Lefaivre J, Barlet J P

机构信息

INRA Theix, St Genès-Champanelle, France.

出版信息

Acta Endocrinol (Copenh). 1992 May;126(5):430-3. doi: 10.1530/acta.0.1260430.

Abstract

Four young milk-fed calves were fitted with catheters chronically implanted in the mesenteric, portal and hepatic veins and in the hepatic artery. Electromagnetic blood flow probes in the portal vein and hepatic artery allowed continuous measurement of hepatic IGF-1 production. In accordance with a latin square design these calves received iv mesenteric infusion (for 60 min) of calcium (Ca, 0.125 mmol.kg body wt-1), the synthetic human parathyroid hormone-related protein (1-34) fragment (PTHrP, 1 nmol.kg body wt-1), the synthetic analogue [tyr]34-bovine PTH-(7-34) NH2 (2 nmol.kg body wt-1) and PTHrP (1 nmol.kg body wt-1) or solvent alone (1.2 ml.kg body wt-1). Hypercalcaemia observed following Ca infusion had no significant effect on hepatic IGF-1 production. PTHrP induced a slight but significant increase in plasma Ca and IGF-1 concentrations measured in the hepatic vein, without changing blood flows measured in the hepatic artery and portal vein. Thus PTHrP increased hepatic IGF-1 production (15.1 +/- 2.7 nmol.6 h-1.kg body wt-1 vs 4 +/- 1.3 nmol.6 h-1.kg body wt-1 in controls; p less than 0.05). These effects induced by PTHrP were inhibited by the synthetic analogue [tyr]34-bPTH-(7-34) NH2.

摘要

对四头以牛奶喂养的幼龄小牛长期植入导管,使其分别位于肠系膜静脉、门静脉、肝静脉以及肝动脉中。门静脉和肝动脉中的电磁血流探头可对肝脏中胰岛素样生长因子-1(IGF-1)的生成进行连续测量。按照拉丁方设计,这些小牛接受了静脉内肠系膜输注(持续60分钟),输注物质分别为钙(Ca,0.125 mmol·kg体重-1)、合成人甲状旁腺激素相关蛋白(1-34)片段(PTHrP,1 nmol·kg体重-1)、合成类似物[tyr]34-牛甲状旁腺激素-(7-34) NH2(2 nmol·kg体重-1)以及PTHrP(1 nmol·kg体重-1)或仅输注溶剂(1.2 ml·kg体重-1)。钙输注后出现的高钙血症对肝脏IGF-1的生成无显著影响。PTHrP使肝静脉中测得的血浆钙和IGF-1浓度出现轻微但显著的升高,而肝动脉和门静脉中测得的血流未发生变化。因此,PTHrP增加了肝脏IGF-1的生成(对照组为4±1.3 nmol·6 h-1·kg体重-1,PTHrP组为15.1±2.7 nmol·6 h-1·kg体重-1;p<0.05)。PTHrP所诱导的这些效应被合成类似物[tyr]34-bPTH-(7-34) NH2抑制。

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