The objective of this study was to investigate the role of palmitoylethanolamide (PEA) in the regulation of energy homeostasis in goldfish (Carassius auratus). We examined the effects of acute or chronic intraperitoneal treatment with PEA (20 μg·g-1 body weight) on parameters related to food intake and its regulatory mechanisms, locomotor activity, glucose and lipid metabolism, and the possible involvement of transcription factors and clock genes on metabolic changes in the liver. Acute PEA treatment induced a decrease in food intake at 6 and 8 h post-injection, comparable to that observed in mammals. This PEA anorectic effect in goldfish could be mediated through interactions with leptin and NPY, as PEA increased hepatic expression of leptin aI and reduced hypothalamic expression of npy. The PEA chronic treatment reduced weight gain, growth rate, and locomotor activity. The rise in glycolytic potential together with the increased potential of glucose to be transported into liver suggests an enhanced use of glucose in the liver after PEA treatment. In addition, part of glucose may be exported to be used in other tissues. The activity of fatty acid synthase (FAS) increased after chronic PEA treatment, suggesting an increase in the hepatic lipogenic capacity, in contrast with the mammalian model. Such lipogenic increment could be linked with the PEA-induction of REV-ERBα and BMAL1 found after the chronic treatment. As a whole, the present study shows the actions of PEA in several compartments related to energy homeostasis and feeding behavior, supporting a regulatory role for this N-acylethanolamine in fish.

中文翻译：

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关于棕榈酰乙醇酰胺在鱼类能量稳态中的作用的第一个证据。

这项研究的目的是调查棕榈酰乙醇酰胺（PEA）在调节金鱼（Car鱼）能量稳态中的作用。我们检查了PEA（20μg·g-1体重）的急性或慢性腹膜内治疗对与食物摄入及其调节机制，运动能力，葡萄糖和脂质代谢以及转录因子和时钟可能涉及的参数有关的影响肝脏代谢变化的基因。与在哺乳动物中观察到的情况相比较，急性PEA处理在注射后6和8 h导致食物摄入减少。PEA在金鱼中的厌食作用可以通过与瘦素和NPY的相互作用来介导，因为PEA可以增加肝中瘦素aI的肝脏表达并降低下丘脑npy的表达。PEA长期治疗可减轻体重增加，生长速度，和运动活动。糖酵解潜能的增加以及葡萄糖向肝脏转运的潜能的增加表明，PEA治疗后肝脏中葡萄糖的利用增加。另外，一部分葡萄糖可以输出以用于其他组织。与哺乳动物模型相比，慢性PEA治疗后脂肪酸合酶（FAS）的活性增加，表明肝脏脂肪生成能力增加。这种脂肪形成的增加可能与慢性治疗后发现的PEA诱导的REV-ERBα和BMAL1有关。总体而言，本研究显示了PEA在与能量稳态和摄食行为有关的多个区室中的作用，支持了该N-酰基乙醇胺在鱼类中的调节作用。糖酵解潜能的增加以及葡萄糖向肝脏转运的潜能的增加表明，PEA治疗后肝脏中葡萄糖的利用增加。另外，一部分葡萄糖可以输出以用于其他组织。与哺乳动物模型相比，慢性PEA治疗后脂肪酸合酶（FAS）的活性增加，表明肝脏脂肪生成能力增加。这种脂肪生成的增加可能与慢性治疗后发现的PEA诱导的REV-ERBα和BMAL1有关。总体而言，本研究显示了PEA在与能量稳态和摄食行为有关的多个区室中的作用，支持了该N-酰基乙醇胺在鱼类中的调节作用。糖酵解潜能的增加以及葡萄糖向肝脏转运的潜能的增加表明，PEA治疗后肝脏中葡萄糖的利用增加。另外，一部分葡萄糖可以输出以用于其他组织。与哺乳动物模型相比，慢性PEA治疗后脂肪酸合酶（FAS）的活性增加，表明肝脏脂肪生成能力增加。这种脂肪生成的增加可能与慢性治疗后发现的PEA诱导的REV-ERBα和BMAL1有关。总体而言，本研究显示了PEA在与能量稳态和摄食行为有关的多个区室中的作用，支持了该N-酰基乙醇胺在鱼类中的调节作用。