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单磷酸腺苷激活蛋白激酶信号传导调节红耳龟对盐度胁迫的脂质代谢

Adenosine Monophosphate-Activated Protein Kinase Signaling Regulates Lipid Metabolism in Response to Salinity Stress in the Red-Eared Slider Turtle .

作者信息

Hong Meiling, Li Na, Li Jiangyue, Li Weihao, Liang Lingyue, Li Qian, Wang Runqi, Shi Haitao, Storey Kenneth B, Ding Li

机构信息

Ministry of Education Key Laboratory for Ecology of Tropical Islands, College of Life Sciences, Hainan Normal University, Haikou, China.

Chengdu Institute of Biology, Chinese Academy of Sciences, Chengdu, China.

出版信息

Front Physiol. 2019 Jul 31;10:962. doi: 10.3389/fphys.2019.00962. eCollection 2019.

DOI:10.3389/fphys.2019.00962
PMID:31417422
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6684833/
Abstract

Aquatic animals have developed various mechanisms to live in either hyperionic or hypoionic environments, and, as such, not many species are capable of surviving in both. The red-eared slider turtle, , a well-known freshwater species, has recently been found to invade and inhabit brackish water. Herein, we focus on some of the metabolic adaptations that are required to survive and cope with salinity stress. The regulation of the adenosine monophosphate (AMP)-activated protein kinase (AMPK), a main cellular "energy sensor," and its influence on lipid metabolism were evaluated with a comparison of three groups of turtles: controls in freshwater, and turtles held in water of either 5‰ salinity (S5) or 15‰ salinity (S15) with sampling at 6, 24, and 48 h and 30 days of exposure. When subjected to elevated salinities of 5 or 15‰, mRNA levels and AMPK enzyme activity increased strongly. In addition, the high expression of the peroxisome proliferator activated receptor-α () transcription factor that, in turn, facilitated upregulation of target genes including carnitine palmitoyltransferase () and acyl-CoA oxidase (). Furthermore, the expression of transcription factors involved in lipid synthesis such as the carbohydrate-responsive element-binding protein () and sterol regulatory element-binding protein 1c () was inhibited, and two of their target genes, acetyl-CoA carboxylase () and fatty acid synthase (), were significantly decreased. Moreover, exposure to saline environments also increased plasma triglyceride (TG) content. Interestingly, the content of low-density lipoprotein cholesterol (LDL-C) and total cholesterol (TC) in plasma was markedly higher than the control in the S15 group after 30 days, which indicated that lipid metabolism was disrupted by chronic exposure to high salinity. These findings demonstrate that activation of AMPK might regulate lipid metabolism in response to salinity stress through the inhibition of lipid synthesis and promotion of lipid oxidation in the liver of . This may be an important component of the observed salinity tolerance of these turtles that allow for invasion of brackish waters.

摘要

水生动物已经发展出各种机制来适应高渗或低渗环境,因此,能够在两种环境中生存的物种并不多。红耳龟是一种著名的淡水物种,最近被发现能够侵入并栖息在半咸水中。在此,我们重点关注红耳龟在生存和应对盐度胁迫时所需的一些代谢适应性变化。通过比较三组龟来评估主要细胞“能量传感器”——腺苷单磷酸(AMP)激活的蛋白激酶(AMPK)的调节及其对脂质代谢的影响:淡水对照组,以及分别饲养在盐度为5‰(S5)或15‰(S15)的水中的龟,在暴露6、24、48小时和30天时进行采样。当盐度升高到5‰或15‰时,AMPK的mRNA水平和酶活性显著增加。此外,过氧化物酶体增殖物激活受体-α(PPAR-α)转录因子的高表达,进而促进了包括肉碱棕榈酰转移酶1(CPT1)和酰基辅酶A氧化酶(ACOX)在内的靶基因的上调。此外,参与脂质合成的转录因子如碳水化合物反应元件结合蛋白(ChREBP)和固醇调节元件结合蛋白1c(SREBP-1c)的表达受到抑制,它们的两个靶基因乙酰辅酶A羧化酶(ACC)和脂肪酸合酶(FAS)也显著降低。此外,暴露于盐环境还会增加血浆甘油三酯(TG)含量。有趣的是,30天后,S15组血浆中低密度脂蛋白胆固醇(LDL-C)和总胆固醇(TC)的含量明显高于对照组,这表明长期暴露于高盐度会扰乱脂质代谢。这些发现表明,AMPK的激活可能通过抑制脂质合成和促进红耳龟肝脏中的脂质氧化来调节对盐度胁迫的脂质代谢。这可能是这些龟能够耐受盐度并侵入半咸水的重要机制之一。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999a/6684833/b59d941bae38/fphys-10-00962-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999a/6684833/79cbb02d073d/fphys-10-00962-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999a/6684833/a35226ad1e69/fphys-10-00962-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999a/6684833/1f3e60a28dbb/fphys-10-00962-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999a/6684833/aa540917c68d/fphys-10-00962-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999a/6684833/646e46511af4/fphys-10-00962-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999a/6684833/b59d941bae38/fphys-10-00962-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999a/6684833/79cbb02d073d/fphys-10-00962-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999a/6684833/d0571479c9a2/fphys-10-00962-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999a/6684833/a35226ad1e69/fphys-10-00962-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999a/6684833/1f3e60a28dbb/fphys-10-00962-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/999a/6684833/b59d941bae38/fphys-10-00962-g007.jpg

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