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Li JM, Li LY, Qin X, et al. Inhibited Carnitine Synthesis Causes Systemic Alteration of Nutrient Metabolism in Zebrafish. Front Physiol. 2018;9:509doi: 10.3389/fphys.2018.00509.
Li, J. M., Li, L. Y., Qin, X., Degrace, P., Demizieux, L., Limbu, S. M., Wang, X., Zhang, M. L., Li, D. L., & Du, Z. Y. (2018). Inhibited Carnitine Synthesis Causes Systemic Alteration of Nutrient Metabolism in Zebrafish. Frontiers in physiology, 9509. https://doi.org/10.3389/fphys.2018.00509
Li, Jia-Min, et al. "Inhibited Carnitine Synthesis Causes Systemic Alteration of Nutrient Metabolism in Zebrafish." Frontiers in physiology vol. 9 (2018): 509. doi: https://doi.org/10.3389/fphys.2018.00509
Li JM, Li LY, Qin X, Degrace P, Demizieux L, Limbu SM, Wang X, Zhang ML, Li DL, Du ZY. Inhibited Carnitine Synthesis Causes Systemic Alteration of Nutrient Metabolism in Zebrafish. Front Physiol. 2018 May 09;9:509. doi: 10.3389/fphys.2018.00509. eCollection 2018. PMID: 29867554; PMCID: PMC5954090.
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Front Physiol. 2018 May 09;9:509. doi: 10.3389/fphys.2018.00509. eCollection 2018.

Inhibited Carnitine Synthesis Causes Systemic Alteration of Nutrient Metabolism in Zebrafish.

Frontiers in physiology

Jia-Min Li, Ling-Yu Li, Xuan Qin, Pascal Degrace, Laurent Demizieux, Samwel M Limbu, Xin Wang, Mei-Ling Zhang, Dong-Liang Li, Zhen-Yu Du

Affiliations

  1. Laboratory of Aquaculture Nutrition and Environmental Health, School of Life Sciences, East China Normal University, Shanghai, China.
  2. Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, China.
  3. Team Pathophysiology of Dyslipidemia, Faculty of Sciences Gabriel, INSERM UMR1231 "Lipides, Nutrition, Cancer," Université Bourgogne Franche-Comté, Dijon, France.
  4. Department of Aquatic Sciences and Fisheries Technology, University of Dar es Salaam, Dar es Salaam, Tanzania.

PMID: 29867554 PMCID: PMC5954090 DOI: 10.3389/fphys.2018.00509

Abstract

Impaired mitochondrial fatty acid β-oxidation has been correlated with many metabolic syndromes, and the metabolic characteristics of the mammalian models of mitochondrial dysfunction have also been intensively studied. However, the effects of the impaired mitochondrial fatty acid β-oxidation on systemic metabolism in teleost have never been investigated. In the present study, we established a low-carnitine zebrafish model by feeding fish with mildronate as a specific carnitine synthesis inhibitor [0.05% body weight (BW)/d] for 7 weeks, and the systemically changed nutrient metabolism, including carnitine and triglyceride (TG) concentrations, fatty acid (FA) β-oxidation capability, and other molecular and biochemical assays of lipid, glucose, and protein metabolism, were measured. The results indicated that mildronate markedly decreased hepatic carnitine concentrations while it had no effect in muscle. Liver TG concentrations increased by more than 50% in mildronate-treated fish. Mildronate decreased the efficiency of liver mitochondrial β-oxidation, increased the hepatic mRNA expression of genes related to FA β-oxidation and lipolysis, and decreased the expression of lipogenesis genes. Mildronate decreased whole body glycogen content, increased glucose metabolism rate, and upregulated the expression of glucose uptake and glycolysis genes. Mildronate also increased whole body protein content and hepatic mRNA expression of mechanistic target of rapamycin (

Keywords: FA β-oxidation; dyslipidemia; low carnitine zebrafish; metabolism; mildronate

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