Mosa Rasha Mofeed Habeeb, Zhang Zhen, Shao Renfu, Deng Chao, Chen Jiezhong, Chen Chen
School of Biomedical Sciences, University of Queensland, St Lucia, QLD, 4072, Australia.
Endocrine. 2015 Jun;49(2):307-23. doi: 10.1007/s12020-015-0531-z. Epub 2015 Feb 4.
Ghrelin and its synthetic analog hexarelin are specific ligands of growth hormone secretagogue (GHS) receptor. GHS have strong growth hormone-releasing effect and other neuroendocrine activities such as stimulatory effects on prolactin and adrenocorticotropic hormone secretion. Recently, several studies have reported other beneficial functions of GHS that are independent of GH. Ghrelin and hexarelin, for examples, have been shown to exert GH-independent cardiovascular activity. Hexarelin has been reported to regulate peroxisome proliferator-activated receptor gamma (PPAR-γ) in macrophages and adipocytes. PPAR-γ is an important regulator of adipogenesis, lipid metabolism, and insulin sensitization. Ghrelin also shows protective effects on beta cells against lipotoxicity through activation of phosphatidylinositol-3 kinase/protein kinase B, c-Jun N-terminal kinase (JNK) inhibition, and nuclear exclusion of forkhead box protein O1. Acylated ghrelin (AG) and unacylated ghrelin (UAG) administration reduces glucose levels and increases insulin-producing beta cell number, and insulin secretion in pancreatectomized rats and in newborn rats treated with streptozotocin, suggesting a possible role of GHS in pancreatic regeneration. Therefore, the discovery of GHS has opened many new perspectives in endocrine, metabolic, and cardiovascular research areas, suggesting the possible therapeutic application in diabetes and diabetic complications especially diabetic cardiomyopathy. Here, we review the physiological roles of ghrelin and hexarelin in the protection and regeneration of beta cells and their roles in the regulation of insulin release, glucose, and fat metabolism and present their potential therapeutic effects in the treatment of diabetes and diabetic-associated heart diseases.
胃饥饿素及其合成类似物六肽生长激素释放肽是生长激素促分泌素(GHS)受体的特异性配体。GHS具有强大的生长激素释放作用以及其他神经内分泌活性,如对催乳素和促肾上腺皮质激素分泌的刺激作用。最近,多项研究报道了GHS的其他有益功能,这些功能独立于生长激素。例如,胃饥饿素和六肽生长激素释放肽已被证明具有不依赖生长激素的心血管活性。据报道,六肽生长激素释放肽可调节巨噬细胞和脂肪细胞中的过氧化物酶体增殖物激活受体γ(PPAR-γ)。PPAR-γ是脂肪生成、脂质代谢和胰岛素敏感性的重要调节因子。胃饥饿素还通过激活磷脂酰肌醇-3激酶/蛋白激酶B、抑制c-Jun氨基末端激酶(JNK)以及叉头框蛋白O1的核排除,对β细胞具有抗脂毒性的保护作用。给予酰基化胃饥饿素(AG)和未酰基化胃饥饿素(UAG)可降低胰腺切除大鼠和链脲佐菌素处理的新生大鼠的血糖水平,并增加胰岛素分泌β细胞数量和胰岛素分泌,提示GHS在胰腺再生中可能发挥作用。因此,GHS的发现为内分泌、代谢和心血管研究领域开辟了许多新的视角,表明其在糖尿病及糖尿病并发症尤其是糖尿病心肌病中的潜在治疗应用。在此,我们综述胃饥饿素和六肽生长激素释放肽在β细胞保护和再生中的生理作用,以及它们在调节胰岛素释放、葡萄糖和脂肪代谢中的作用,并介绍它们在治疗糖尿病和糖尿病相关心脏病中的潜在治疗效果。