Song Xixi, Wang Minghui, Jiao Hongchao, Zhao Jingpeng, Wang Xiaojuan, Lin Hai
College of Animal Science and Veterinary Medicine, Shandong Agricultural University, No. 61 Daizong Street, Tai'an 271018, China; School of Sport Social Science, Shandong Sport University, No. 10600 Shiji Street, Jinan 250100, China.
College of Animal Science and Veterinary Medicine, Shandong Agricultural University, No. 61 Daizong Street, Tai'an 271018, China.
Biochim Biophys Acta Mol Cell Biol Lipids. 2022 Feb;1867(2):159081. doi: 10.1016/j.bbalip.2021.159081. Epub 2021 Nov 30.
Ghrelin, classically known as a central appetite-stimulating hormone, has recently been recognized to play an important role in peripheral tissue energy metabolism. In chicken, contrary to mammal, ghrelin acts as an anorexia signal, increased by fasting and further elevated after refed. In the present study, the effect of ghrelin on glucose/lipid utilization by peripheral tissues was investigated. Injection of exogenous acyl ghrelin reduced plasma triglyceride and glucose levels of chickens at both fasting and fed status. In the in vitro cultured chicken primary hepatocytes, adipocytes, and myoblasts, ghrelin suppressed glucose uptake, stimulated fatty acids uptake and oxidation, and decreased TG content. In hepatocyte, ghrelin increased the activities of LPL and HL, and upregulated the expression levels of gene ACC, CPT1, and PPARα. Ghrelin treatment markedly increased the protein level of p-ACC, PPARγ, PGC1α, and CPT1 in hepatocytes, adipocytes and myoblasts. Inhibition of AMPK activity by Compound C had no influence on glucose uptake by hepatocyte, adipocyte, and myoblast, but further amplified the stimulated fatty acid uptake of adipocyte by ghrelin. The present result demonstrates that ghrelin facilitates the uptake and oxidation of fatty acid and cut down the utilization of glucose by the liver, muscle, and adipose tissues. The result suggests that ghrelin functions as a signal of fatty acid oxidation. The study provides a vital framework for understanding the intrinsic role of ghrelin as a crucial factor in the concerted regulation of metabolic substrate of hepatocytes, adipocytes, and myoblasts.
胃饥饿素，传统上被认为是一种中枢性食欲刺激激素，最近被认识到在周围组织能量代谢中发挥重要作用。在鸡中，与哺乳动物相反，胃饥饿素作为一种厌食信号，在禁食时增加，并在重新喂食后进一步升高。在本研究中，研究了胃饥饿素对周围组织葡萄糖/脂质利用的影响。注射外源性酰基胃饥饿素可降低禁食和进食状态下鸡的血浆甘油三酯和葡萄糖水平。在体外培养的鸡原代肝细胞、脂肪细胞和成肌细胞中，胃饥饿素抑制葡萄糖摄取，刺激脂肪酸摄取和氧化，并降低甘油三酯含量。在肝细胞中，胃饥饿素增加脂蛋白脂肪酶（LPL）和肝脂酶（HL）的活性，并上调乙酰辅酶A羧化酶（ACC）、肉碱棕榈酰转移酶1（CPT1）和过氧化物酶体增殖物激活受体α（PPARα）的基因表达水平。胃饥饿素处理显著增加了肝细胞、脂肪细胞和成肌细胞中磷酸化ACC、PPARγ、过氧化物酶体增殖物激活受体γ共激活因子1α（PGC1α）和CPT1的蛋白水平。用化合物C抑制AMPK活性对肝细胞、脂肪细胞和成肌细胞的葡萄糖摄取没有影响，但进一步放大了胃饥饿素对脂肪细胞脂肪酸摄取的刺激作用。目前的结果表明，胃饥饿素促进肝脏、肌肉和脂肪组织对脂肪酸的摄取和氧化，并减少葡萄糖的利用。结果表明，胃饥饿素作为脂肪酸氧化的信号发挥作用。该研究为理解胃饥饿素作为肝细胞、脂肪细胞和成肌细胞代谢底物协同调节的关键因素的内在作用提供了重要框架。
