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糖尿病大鼠胃肠道、肠系膜血管和肝门静脉前列腺素合成的差异变化:配对喂养与随意进食的比较

Differential changes of prostanoid synthesis by the gastrointestinal tract, mesenteric vasculature and hepatic portal vein of diabetic rats: comparison between pair and ad libitum feeding.

作者信息

Jeremy J Y, Thompson C S, Mikhailidis D P

机构信息

Department of Chemical Pathology and Human Metabolism, Royal Free Hospital and School of Medicine, London, England.

出版信息

In Vivo. 1992 Nov-Dec;6(6):635-9.

PMID:1296814
Abstract

The synthesis of the prostaglandins (PG) I2 (measured as 6-oxo-PGF1 alpha), E2, E2 alpha) and thromboxane (TX) A2 (measured as TXB2) by the mucosal and muscular portions of the stomach, duodenum, jejunum, ileum, mesenteric vessels, hepatic portal vein and two arteries (carotid and aorta) was investigated in long term streptozotocin-induced diabetes mellitus (DM; fed ad libitum and pair fed). In all regions of the gastrointestinal tract there were no changes in PG synthesis (per unit weight of tissue) in diabetic rats (pair fed or fed ad libitum) compared to controls. However, there were marked increases in PG synthesis (up to 3 fold) by the mesenteric vasculature and hepatic portal vein in diabetic animals fed ad libitum and in pair fed diabetic rats and decreases in the aorta and carotid artery. These data suggest that increases in PG synthesis by the splanchnic vasculature may constitute a specific adaptive response to DM. The similarity of the responses of pair fed rats to those of rats fed ad libitum indicates that DM and not hyperphagia is the likely determinant of these adaptive changes. Given that increased splanchnic blood flow enhances nutrient uptake (both known to occur in DM), the increase in splanchnic vascular PG synthesis, in particular of vasodilatory PGI2, may contribute to enhanced nutrient uptake.

摘要

在长期链脲佐菌素诱导的糖尿病(DM;自由采食和配对喂食)模型中,研究了胃、十二指肠、空肠、回肠、肠系膜血管、肝门静脉以及两条动脉(颈动脉和主动脉)的黏膜和肌层部分合成前列腺素(PG)I2(以6-氧代-PGF1α衡量)、E2、E2α以及血栓素(TX)A2(以TXB2衡量)的情况。与对照组相比,糖尿病大鼠(配对喂食或自由采食)胃肠道所有区域的PG合成(每单位组织重量)均无变化。然而,自由采食的糖尿病动物以及配对喂食的糖尿病大鼠的肠系膜血管和肝门静脉的PG合成显著增加(高达3倍),而主动脉和颈动脉的PG合成则减少。这些数据表明,内脏血管PG合成增加可能是对DM的一种特异性适应性反应。配对喂食大鼠与自由采食大鼠反应的相似性表明,这些适应性变化的可能决定因素是DM而非摄食过多。鉴于内脏血流量增加会增强营养物质摄取(这两者在DM中均会发生),内脏血管PG合成增加,尤其是血管舒张性PGI2的增加,可能有助于增强营养物质摄取。

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