Salmerón Cristina, Johansson Marcus, Asaad Maryam, Angotzi Anna R, Rønnestad Ivar, Stefansson Sigurd O, Jönsson Elisabeth, Björnsson Björn Thrandur, Gutiérrez Joaquim, Navarro Isabel, Capilla Encarnación
Department of Physiology and Immunology, Faculty of Biology, University of Barcelona, Barcelona 08028, Spain.
Fish Endocrinology Laboratory, Department of Biological and Environmental Sciences, University of Gothenburg, Gothenburg 40590, Sweden.
Comp Biochem Physiol A Mol Integr Physiol. 2015 Oct;188:40-8. doi: 10.1016/j.cbpa.2015.06.017. Epub 2015 Jun 20.
Leptin and ghrelin are important regulators of energy homeostasis in mammals, whereas their physiological roles in fish have not been fully elucidated. In the present study, the effects of leptin and ghrelin on adipogenesis, lipolysis and on expression of lipid metabolism-related genes were examined in rainbow trout adipocytes in vitro. Leptin expression and release increased from preadipocytes to mature adipocytes in culture, but did not affect the process of adipogenesis. While ghrelin and its receptor were identified in cultured differentiated adipocytes, ghrelin did not influence either preadipocyte proliferation or differentiation, indicating that it may have other adipose-related roles. Leptin and ghrelin increased lipolysis in mature freshly isolated adipocytes, but mRNA expression of lipolysis markers was not significantly modified. Leptin significantly suppressed the fatty acid transporter-1 expression, suggesting a decrease in fatty acid uptake and storage, but did not affect expression of any of the lipogenesis or β-oxidation genes studied. Ghrelin significantly increased the mRNA levels of lipoprotein lipase, fatty acid synthase and peroxisome proliferator-activated receptor-β, and thus appears to stimulate synthesis of triglycerides as well as their mobilization. Overall, the study indicates that ghrelin, but not leptin seems to be an enhancer of lipid turn-over in adipose tissue of rainbow trout, and this regulation may at least partly be mediated through autocrine/paracrine mechanisms. The mode of action of both hormones needs to be further explored to better understand their roles in regulating adiposity in fish.
瘦素和胃饥饿素是哺乳动物能量平衡的重要调节因子，而它们在鱼类中的生理作用尚未完全阐明。在本研究中，我们在体外对虹鳟脂肪细胞中瘦素和胃饥饿素对脂肪生成、脂肪分解以及脂质代谢相关基因表达的影响进行了检测。培养过程中，瘦素的表达和释放从前脂肪细胞到成熟脂肪细胞逐渐增加，但不影响脂肪生成过程。虽然在培养的分化脂肪细胞中鉴定出了胃饥饿素及其受体，但胃饥饿素既不影响前脂肪细胞的增殖也不影响其分化，这表明它可能具有其他与脂肪相关的作用。瘦素和胃饥饿素可增加新鲜分离的成熟脂肪细胞的脂肪分解，但脂肪分解标志物的mRNA表达没有明显改变。瘦素显著抑制脂肪酸转运蛋白1的表达，表明脂肪酸摄取和储存减少，但不影响所研究的任何脂肪生成或β-氧化基因的表达。胃饥饿素显著增加脂蛋白脂肪酶、脂肪酸合酶和过氧化物酶体增殖物激活受体-β的mRNA水平，因此似乎既能刺激甘油三酯的合成又能促进其动员。总体而言，该研究表明，胃饥饿素而非瘦素似乎是虹鳟脂肪组织中脂质周转的增强剂之一，并且这种调节可能至少部分通过自分泌/旁分泌机制介导。两种激素的作用方式都需要进一步探索，以更好地了解它们在调节鱼类肥胖中的作用。
