Schusdziarra V
Scand J Gastroenterol Suppl. 1983;82:69-84.
Somatostatin was originally isolated from the hypothalamus and has now been found in large quantities in the gastrointestinal tract and pancreas. Its localisation in nerve endings and endocrine-like cells suggests that somatostatin is a putative neurotransmitter and/or neuromodulator, local or paracrine acting substance and true endocrine factor or hormone. The present communication summarises the evidence for the release of somatostatin into the gastrointestinal lumen and the potential action of luminally released somatostatin. Furthermore, the evidence is presented for the release of splanchnic somatostatin into the circulation in response to a meal in rat, dog and man. The biological role of postprandially released and circulating somatostatin is to prevent an exaggerated response of certain exo- and/or endocrine functions of the gastrointestinal tract and pancreas as indicated by studies employing low-dose infusions of synthetic somatostatin or by neutralisation of somatostatin following the injection of specific antibodies. The release of gastric and pancreatic somatostatin is regulated by ingested and circulating nutrients and is modulated by neural mechanisms (cholinergic, adrenergic, dopaminergic) histamine, prostaglandins, opiates and gastrointestinal hormones. Several studies demonstrating a tight interaction between somatostatin and insulin indicate that insulin is another important factor in the regulation of basal and postprandial somatostatin release. The role of somatostatin in pathophysiological states such as peptic ulceration and diabetes mellitus is not entirely clear but the present evidence indicates that alterations of tissue somatostatin content or plasma somatostatin levels are secondary to changes of other factors (increased gastric acid secretion, insulin deficiency) rather than representing the primary cause for the underlying disease. Measurements of somatostatin in plasma are useful as a marker for the diagnosis of somatostatin-producing tumours.
生长抑素最初是从下丘脑分离出来的，现在已在胃肠道和胰腺中大量发现。它在神经末梢和内分泌样细胞中的定位表明，生长抑素是一种假定的神经递质和/或神经调节剂、局部或旁分泌作用物质以及真正的内分泌因子或激素。本通讯总结了生长抑素释放到胃肠道腔中的证据以及腔内释放的生长抑素的潜在作用。此外，还提供了大鼠、狗和人进食后内脏生长抑素释放到循环中的证据。餐后释放和循环的生长抑素的生物学作用是防止胃肠道和胰腺的某些外分泌和/或内分泌功能出现过度反应，这一点已通过使用低剂量合成生长抑素输注或注射特异性抗体后中和生长抑素的研究得到证实。胃和胰腺生长抑素的释放受摄入和循环中的营养物质调节，并受神经机制（胆碱能、肾上腺素能、多巴胺能）、组胺、前列腺素、阿片类药物和胃肠激素的调节。多项研究表明生长抑素与胰岛素之间存在紧密的相互作用，这表明胰岛素是调节基础和餐后生长抑素释放的另一个重要因素。生长抑素在消化性溃疡和糖尿病等病理生理状态中的作用尚不完全清楚，但目前的证据表明，组织生长抑素含量或血浆生长抑素水平的改变是其他因素（胃酸分泌增加、胰岛素缺乏）变化的继发结果，而不是潜在疾病的主要原因。测量血浆中的生长抑素可作为诊断生长抑素产生肿瘤的标志物。
