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

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, Trachemys scripta elegans, a well-known freshwater species, has recently been found to invade and in...

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Bibliographic Details
Published in:Frontiers in Physiology
Main Authors: Hong, Meiling, Li, Na, Li, Jiangyue, Li, Weihao, Liang, Lingyue, Li, Qian, Wang, Runqi, Shi, Haitao, Storey, Kenneth B., Ding, Li
Format: Report
Language:English
Published: FRONTIERS MEDIA SA 2019
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Online Access:http://ir.imde.ac.cn/handle/131551/26806
https://doi.org/10.3389/fphys.2019.00962
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Summary: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, Trachemys scripta elegans, 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 parts per thousand salinity (S5) or 15 parts per thousand salinity (S15) with sampling at 6, 24, and 48 h and 30 days of exposure. When subjected to elevated salinities of 5 or 15 parts per thousand, AMPK mRNA levels and AMPK enzyme activity increased strongly. In addition, the high expression of the peroxisome proliferator activated receptor-alpha (PPAR alpha) transcription factor that, in turn, facilitated upregulation of target genes including carnitine palmitoyltransferase (CPT) and acyl-CoA oxidase (ACO). Furthermore, the expression of transcription factors involved in lipid synthesis such as the carbohydrate-responsive element-binding protein (ChREBP) and sterol regulatory element-binding protein 1c (SREBP-1c) was inhibited, and two of their target genes, acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), 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 ...