未酰化的以及酰化的胃饥饿素均可促进HIT-T15胰腺β细胞的存活并抑制其凋亡。
Unacylated as well as acylated ghrelin promotes cell survival and inhibit apoptosis in HIT-T15 pancreatic beta-cells.
作者信息
Granata R, Settanni F, Trovato L, Destefanis S, Gallo D, Martinetti M, Ghigo E, Muccioli G
机构信息
Laboratory of Molecular and Cellular Endocrinology, Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Turin, Turin, Italy.
出版信息
J Endocrinol Invest. 2006 Oct;29(9):RC19-22. doi: 10.1007/BF03347367.
Ghrelin is mainly produced by the stomach, although it is expressed in other tissues, including the pancreas. Among its pleiotropic actions, ghrelin prevents the development of diabetes in rats and exerts mitogenic and antiapoptotic effects in different cell types. In addition, a ghrelin-producing epsilon-cell population has been demonstrated in rodent islets, suggesting a direct role in the control of islet cell survival. In this study, we investigated the effect of acylated ghrelin (AG) and unacylated ghrelin (UAG) on cell survival of HIT-T15 pancreatic beta cells. We show that both AG and UAG equally prevented beta cell death induced by serum withdrawal. In addition, both peptides inhibited serum starvation-induced apoptosis. These findings indicate that UAG and AG prevent cell death and apoptosis of pancreatic beta cells. Since only AG, but not UAG, binds the GRLN receptor, a different and as yet unknown receptor is likely involved in these survival mechanisms.
胃饥饿素主要由胃产生，不过它也在包括胰腺在内的其他组织中表达。在其多种作用中，胃饥饿素可预防大鼠患糖尿病，并在不同细胞类型中发挥促有丝分裂和抗凋亡作用。此外，在啮齿动物胰岛中已证实存在产生胃饥饿素的ε细胞群，这表明其在控制胰岛细胞存活方面具有直接作用。在本研究中，我们调查了酰化胃饥饿素（AG）和去酰化胃饥饿素（UAG）对HIT-T15胰腺β细胞存活的影响。我们发现AG和UAG均可同样有效地预防血清撤出诱导的β细胞死亡。此外，这两种肽均抑制血清饥饿诱导的细胞凋亡。这些发现表明UAG和AG可预防胰腺β细胞的细胞死亡和凋亡。由于只有AG而非UAG能与胃饥饿素受体结合，因此这些存活机制可能涉及一种不同的、尚不清楚的受体。
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