Ghrelin (human) was isolated from the gut of both human and rat as the endogenous ligand of the growth hormone secretagogue receptor (GHS-R), and has an effection on the activity of arcute neurones with a much stronger affinity (IC50, 0.3×10-9M) than GHSR antagonist (D-Lys3)-GHRP-6 (IC50, 0.9×10-6M) [1]. The highest levels of ghrelin are secreted from the X/A - like cells of the oxyntic glands located in the gastric fundus, with lower levels widely distributed throughout the body [2]. Ghrelin is secreted direct into the local gastric circulation and transported to the brain directly, requiring it to either cross the blood-brain barrier via a saturated transport system or via the blood stream to enter areas of the brain that are not protected by the blood-brain barrier [3]. Ghrelin modulates the hypothalamic arcuate nucleus, in an indirect manner, via activation of the vagus nerve and brain stem nuclei [4]. Ghrelin has a homeostatic role that encompasses multiple areas of the body, with actions that include downregulation of brown adipose tissue thermogenesis [5-7], modulation of non-hypothalamic brain regions producing an increased taste sensation [7] and stimulation of gastric emptying and motility [8]. The actions of ghrelin may contribute to the development of T2DM and obesity [9].
Differentiating visceral adipocytes were exposed to increasing concentrations of acylated (human) and desacyl ghrelin (0.1-1000 pmol l-1) for 48 h, and induced a significant increase in PPARG and SREBF1 transcript levels, the proportion of cells positive for lipid droplets was markedly increased in the presence of both ghrelin forms, compared with the cells in the differentiation medium without ghrelin [10].
References:
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[9]. MÜller T D, Nogueiras R, Andermann M L, et al. Ghrelin[J]. Molecular metabolism, 2015, 4(6): 437-460.
[10]. RodrÍguez A, GÓmez-Ambrosi J, CatalÁn V, et al. Acylated and desacyl ghrelin stimulate lipid accumulation in human visceral adipocytes[J]. International journal of obesity, 2009, 33(5): 541-552.
人类胃泌素（Ghrelin）是从人类和大鼠肠道中分离出来的内源性生长激素分泌素受体（GHS-R）的配体,并对弧形神经元活动产生影响,其亲和力比GHSR拮抗剂（D-Lys3）-GHRP-6强得多（IC50为0.3×10-9M,0.9×10-6M）[1]。胃泌素最高水平的分泌源是位于胃底部酸性腺中的X/A-类细胞,较低水平的分布广泛在全身[2]。胃泌素直接分泌到局部胃循环中,并直接输送到大脑,要求它要么通过饱和的转运系统穿越血脑屏障,要么通过血流进入未受血脑屏障保护的脑部区域[3]。胃泌素通过激活迷走神经和脑干核间接地调节下丘脑弧形核[4]。胃泌素具有涵盖身体多个区域的稳态作用,其作用包括下调棕色脂肪组织的热发生[5-7]、调节非下丘脑的脑区产生增加的味觉感觉[7]以及促进胃排空和运动[8]。胃泌素的作用可能有助于2型糖尿病和肥胖的发展[9]。
将分化的内脏脂肪细胞暴露于逐渐增加的酰化（人）和去酰化胃泌素（0.1-1000 pmol / L）浓度中,持续48小时,结果显示与没有酰化胃泌素的分化培养基相比,PPARG和SREBF1转录水平明显增加,呈现出更多的含脂滴细胞比例增加。[10]