Passier P C, Vullings H G, Diederen J H, Van der Horst D J
Department of Experimental Zoology, Utrecht University, The Netherlands.
J Endocrinol. 1997 May;153(2):299-305. doi: 10.1677/joe.0.1530299.
The effect of trehalose at various concentrations on the release of adipokinetic hormones (AKHs) from the adipokinetic cells in the glandular part of the corpus cardiacum of Locusta migratoria was studied in vitro. Pools of five corpora cardiaca or pools of five glandular parts of corpora cardiaca were incubated in a medium containing different concentrations of trehalose in the absence or presence of AKH-release-inducing agents. It was demonstrated that trehalose inhibits spontaneous release of AKH I in a dose-dependent manner. At a concentration of 80 mM, which is the concentration found in the hemolymph at rest, trehalose significantly decreased the release of AKH I induced by 100 microM locustatachykinin 1, 10 microM 3-isobutyl-1-methylxanthine (IBMX) or high potassium concentrations. The specificity of the effect of trehalose was studied by incubating pools of corpora cardiaca with the non-hydrolyzable disaccharide sucrose or with glucose, the degradation product of trehalose, both in the presence and absence of 10 microM IBMX. Sucrose had no effect at all on the release of AKH I, whereas glucose strongly inhibited its release. The results point to the inhibitory effect of trehalose on the release of AKH I being exerted, at least partly, at the level of the adipokinetic cells, possibly after its conversion into glucose. The data presented in this study support the hypothesis that in vivo the relatively high concentration of trehalose (80 mM) at rest strongly inhibits the release of AKHs. At the onset of flight, the demand for energy substrates exceeds the amount of trehalose that can be mobilized from the fat body and consequently the trehalose concentration in the hemolymph decreases. This relieves the inhibitory effect of trehalose on the release of AKHs, which in turn mobilize lipids from the fat body.
体外研究了不同浓度海藻糖对飞蝗心侧体腺部脂肪动激素（AKHs）分泌细胞释放脂肪动激素的影响。将五个心侧体或五个心侧体腺部放在含有不同浓度海藻糖的培养基中孵育，有无AKH释放诱导剂均可。结果表明，海藻糖以剂量依赖方式抑制AKH I的自发释放。在静息血淋巴中发现的浓度80 mM时，海藻糖显著降低了100 microM蝗虫速激肽1、10 microM 3 - 异丁基 - 1 - 甲基黄嘌呤（IBMX）或高钾浓度诱导的AKH I释放。通过在有无10 microM IBMX的情况下，将心侧体与不可水解的双糖蔗糖或海藻糖降解产物葡萄糖一起孵育，研究了海藻糖作用的特异性。蔗糖对AKH I的释放完全没有影响，而葡萄糖强烈抑制其释放。结果表明，海藻糖对AKH I释放的抑制作用至少部分是在脂肪动激素分泌细胞水平发挥的，可能是在其转化为葡萄糖之后。本研究中的数据支持这样的假设，即体内静息时相对较高浓度的海藻糖（80 mM）强烈抑制AKHs的释放。在飞行开始时，对能量底物的需求超过了可从脂肪体动员的海藻糖量，因此血淋巴中海藻糖浓度降低。这减轻了海藻糖对AKHs释放的抑制作用，进而从脂肪体动员脂质。
