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首页> 外文期刊>International Journal of Molecular Sciences >Goldfish Leptin-AI and Leptin-AII: Function and Central Mechanism in Feeding Control
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Goldfish Leptin-AI and Leptin-AII: Function and Central Mechanism in Feeding Control

机译：金鱼Leptin-AI和Leptin-AII：在饲养控制中的功能和中枢机制

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In mammals, leptin is a peripheral satiety factor that inhibits feeding by regulating a variety of appetite-related hormones in the brain. However, most of the previous studies examining leptin in fish feeding were performed with mammalian leptins, which share very low sequence homologies with fish leptins. To elucidate the function and mechanism of endogenous fish leptins in feeding regulation, recombinant goldfish leptin-AI and leptin-AII were expressed in methylotrophic yeast and purified by immobilized metal ion affinity chromatography (IMAC). By intraperitoneal (IP) injection, both leptin-AI and leptin-AII were shown to inhibit the feeding behavior and to reduce the food consumption of goldfish in 2 h. In addition, co-treatment of leptin-AI or leptin-AII could block the feeding behavior and reduce the food consumption induced by neuropeptide Y (NPY) injection. High levels of leptin receptor ( lepR ) mRNA were detected in the hypothalamus, telencephalon, optic tectum and cerebellum of the goldfish brain. The appetite inhibitory effects of leptins were mediated by downregulating the mRNA levels of orexigenic NPY , agouti-related peptide ( AgRP ) and orexin and upregulating the mRNA levels of anorexigenic cocaine-amphetamine-regulated transcript ( CART ), cholecystokinin ( CCK ), melanin-concentrating hormone ( MCH ) and proopiomelanocortin ( POMC ) in different areas of the goldfish brain. Our study, as a whole, provides new insights into the functions and mechanisms of leptins in appetite control in a fish model.
机译：在哺乳动物中，瘦素是一种外围饱腹感因子，可通过调节大脑中各种与食欲相关的激素来抑制进食。然而，大多数以前在鱼类摄食中研究瘦素的研究都是使用哺乳动物瘦素进行的，而哺乳动物瘦素与鱼瘦素的序列同源性非常低。为了阐明内源鱼瘦素在饲料调节中的功能和机理，在甲基营养酵母中表达重组金鱼瘦素-AI和瘦素-AII，并通过固定金属离子亲和色谱法（IMAC）进行纯化。通过腹膜内（IP）注射，瘦素-AI和瘦素-AII均显示出在2小时内抑制摄食行为并减少了金鱼的食物消耗。此外，瘦素-AI或瘦素-AII的共同处理可能会阻止喂养行为，并减少神经肽Y（NPY）注射引起的食物消耗。在金鱼脑的下丘脑，端脑，视神经顶盖和小脑中检测到高水平的瘦素受体（lepR）mRNA。瘦素的食欲抑制作用是通过下调食源性NPY，古钩相关肽（AgRP）和食欲肽的mRNA水平以及上调食欲的可卡因-苯丙胺调节转录本（CART），胆囊收缩素（CCK），黑色素-mRNA的水平来调节的在金鱼脑的不同区域浓缩激素（MCH）和原黑素皮质激素（POMC）。总体而言，我们的研究为鱼类模型中瘦素在食欲控制中的功能和机制提供了新见解。

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