胃源的辛酸化肽ghrelin于1999年被发现,被认为是生长激素促分泌素受体(GHSR)的内源性激动剂。随后,ghrelin不仅在控制生长激素分泌方面发挥关键作用,还有各种其他生理功能,包括,但不限于,食物摄入量,与奖励相关的行为,葡萄糖稳态和胃肠道运动。重要的是,一种非酰化形式的生长素释放肽,去酰基-生长素释放肽,也可以在生物样品中检测到。去酰基-生长素释放肽,然而,在生理水平上不与GHSR结合,它的生理作用仍然没有ghrelin那么好。Ghrelin和去酰基-ghrelin目前在文献中使用许多不同的术语,强调需要一致的命名法。用于指定ghrelin的术语的可变性不仅会导致混乱,还有误解,特别是对于那些不太熟悉ghrelin文学的人。因此,我们在对ghrelin文献有贡献的专家中进行了一项调查,旨在确定是否可以达成共识。根据这一共识的结果,我们建议使用术语“ghrelin”和“去酰基-ghrelin”来指代激素本身及其非酰化形式,分别。根据这一共识的结果,我们进一步建议使用术语“GHSR”作为受体,和“LEAP2”用于肝脏表达的抗菌肽2,这是一种最近公认的内源性GHSR拮抗剂/反向激动剂。
The stomach-derived octanoylated peptide ghrelin was discovered in 1999 and recognized as an endogenous agonist of the growth hormone secretagogue receptor (GHSR). Subsequently, ghrelin has been shown to play key roles in controlling not only growth hormone secretion, but also a variety of other physiological functions including, but not limited to, food intake, reward-related behaviors, glucose homeostasis and gastrointestinal tract motility. Importantly, a non-acylated form of
ghrelin, desacyl-
ghrelin, can also be detected in biological samples. Desacyl-ghrelin, however, does not bind to GHSR at physiological levels, and its physiological role has remained less well-characterized than that of ghrelin.
Ghrelin and desacyl-
ghrelin are currently referred to in the literature using many different terms, highlighting the need for a consistent nomenclature. The variability of terms used to designate ghrelin can lead not only to confusion, but also to miscommunication, especially for those who are less familiar with the ghrelin literature. Thus, we conducted a survey among experts who have contributed to the ghrelin literature aiming to identify whether a
consensus may be reached. Based on the results of this
consensus, we propose using the terms \"
ghrelin\" and \"desacyl-
ghrelin\" to refer to the hormone itself and its non-acylated form, respectively. Based on the results of this
consensus, we further propose using the terms \"GHSR\" for the receptor, and \"LEAP2\" for liver-expressed antimicrobial peptide 2, a recently recognized endogenous GHSR antagonist/inverse agonist.