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糖尿病对大鼠血浆及外周组织中两种形式甲硫氨酸脑啡肽水平的影响。

Effect of diabetes on the levels of two forms of Met-enkephalin in plasma and peripheral tissues of the rat.

作者信息

Kolta M G, Pierzchala K, Houdi A A, Van Loon G R

机构信息

College of Pharmacy and Pharmaceutical Sciences, Florida A&M University, Tallahassee 32307.

出版信息

Neuropeptides. 1992 Jan;21(1):55-63. doi: 10.1016/0143-4179(92)90152-m.

DOI:10.1016/0143-4179(92)90152-m
PMID:1738434
Abstract

Levels of native and cryptic or peptidase-derivable (after being digested with trypsin and carboxypeptidase) Met-enkephalin were measured by a specific radioimmunoassay method in plasma, anterior and neurointermediate lobes of pituitary and various peripheral tissues of streptozotocin (STZ) diabetic rats. The results show that the highest concentration of native and cryptic Met-enkephalin were found in the neurointermediate lobe of pituitary. Streptozotocine-induced diabetes alters the concentration of either or both forms of Met-enkephalin in plasma, the anterior and neurointermediate lobes of the pituitary, heart, lung, spleen, liver, seminal vesicle, vas deferens, kidney, bladder detrusor, and duodenum. One of the most pronounced effects of diabetes observed in this study is seen in the seminal vesicles where native Met-enkephalin was depleted to less than 10% of the control value. The uneven distribution of Met-enkephalin in peripheral tissues may suggest that these tissues process and/or metabolize Met-enkephalin to different degrees. Our data also suggest that STZ-induced diabetes alters the enkephalinergic activity in some of these tissues. It is suggested that some of the peripheral pathophysiological symptoms associated with diabetes may be attributed, in part, to altered activity of enkephalinergic systems.

摘要

采用特异性放射免疫分析方法,测定了链脲佐菌素(STZ)诱导的糖尿病大鼠血浆、垂体前叶和神经中间叶以及各种外周组织中天然的、隐蔽的或经胰蛋白酶和羧肽酶消化后可衍生出的甲硫氨酸脑啡肽水平。结果显示,垂体神经中间叶中天然和隐蔽的甲硫氨酸脑啡肽浓度最高。链脲佐菌素诱导的糖尿病改变了血浆、垂体前叶和神经中间叶、心脏、肺、脾脏、肝脏、精囊、输精管、肾脏、膀胱逼尿肌和十二指肠中甲硫氨酸脑啡肽两种形式或其中一种形式的浓度。本研究中观察到的糖尿病最显著的影响之一见于精囊,其中天然甲硫氨酸脑啡肽减少至对照值的不到10%。甲硫氨酸脑啡肽在外周组织中的分布不均可能表明这些组织对甲硫氨酸脑啡肽的加工和/或代谢程度不同。我们的数据还表明,STZ诱导的糖尿病改变了其中一些组织中的脑啡肽能活性。提示与糖尿病相关的一些外周病理生理症状可能部分归因于脑啡肽能系统活性的改变。

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