Mitochondrial fatty acid β-oxidation inhibition promotes carbohydrate catabolism and protein deposition through energy homeostasis remodelling. The Journal of Nutrition, nxaa187, https://doi.org/10.1093/jn/nxaa187.

Simple item page
dc.contributor.authorLing-Yu Li
dc.contributor.authorJia-Min Li
dc.contributor.authorLi-Jun Ning
dc.contributor.authorDong-Liang Lu
dc.contributor.authorYuan Luo
dc.contributor.authorQiang Ma
dc.contributor.authorSamwel Mchele Limbu
dc.contributor.authorDong-Liang Li
dc.contributor.authorLi-Qiao Chen
dc.contributor.authorIrfan J. Lodhi
dc.contributor.authorPascal Degrace
dc.contributor.authorMei-Ling Zhang
dc.contributor.authorZhen-Yu Du
dc.date.accessioned2021-04-18T06:50:03Z
dc.date.available2021-04-18T06:50:03Z
dc.date.issued2019-09
dc.description.abstractBackground Fish cannot use carbohydrate efficiently and instead utilize protein for energy supply, thus limiting dietary protein storage. Protein deposition is dependent on protein turnover balance, which correlates tightly with cellular energy homeostasis. Mitochondrial fatty acid β-oxidation (FAO) plays a crucial role in energy metabolism. However, the effect of remodeled energy homeostasis caused by inhibited mitochondrial FAO on protein deposition in fish has not been intensively studied. Objectives This study aimed to identify the regulatory role of mitochondrial FAO in energy homeostasis maintenance and protein deposition by studying lipid, glucose, and protein metabolism in fish. Methods Carnitine-depleted male Nile tilapia (initial weight: 4.29 ± 0.12 g; 3 mo old) were established by feeding them with mildronate diets (1000 mg/kg/d) for 6 wk. Zebrafish deficient in the carnitine palmitoyltransferase 1b gene (cpt1b) were produced by using CRISPR/Cas9 gene-editing technology, and their males (154 ± 3.52 mg; 3 mo old) were used for experiments. Normal Nile tilapia and wildtype zebrafish were used as controls. We assessed nutrient metabolism and energy homeostasis–related biochemical and molecular parameters, and performed 14C-labeled nutrient tracking and transcriptomic analyses. Results The mitochondrial FAO decreased by 33.1–88.9% (liver) and 55.6–68.8% (muscle) in carnitine-depleted Nile tilapia and cpt1b-deficient zebrafish compared with their controls (P < 0.05). Notably, glucose oxidation and muscle protein deposition increased by 20.5–24.4% and 6.40–8.54%, respectively, in the 2 fish models compared with their corresponding controls (P < 0.05). Accordingly, the adenosine 5′-monophosphate–activated protein kinase/protein kinase B–mechanistic target of rapamycin (AMPK/AKT-mTOR) signaling was significantly activated in the 2 fish models with inhibited mitochondrial FAO (P < 0.05). Conclusions These data show that inhibited mitochondrial FAO in fish induces energy homeostasis remodeling and enhances glucose utilization and protein deposition. Therefore, fish with inhibited mitochondrial FAO could have high potential to utilize carbohydrate. Our results demonstrate a potentially new approach for increasing protein deposition through energy homeostasis regulation in cultured animals.en_US
dc.description.sponsorshipNational Key Research and Development Project (2018YFD0900400) and the National Natural Science Fund (31830102 and 31772859)en_US
dc.identifier.citationLing-Yu Li, Jia-Min Li, Li-Jun Ning, Dong-Liang Lu, Yuan Luo, Qiang Ma, Samwel Mchele Limbu, Dong-Liang Li, Li-Qiao Chen, Irfan J. Lodhi, Pascal Degrace, Mei-Ling Zhang and Zhen-Yu Du (2020). Mitochondrial fatty acid β-oxidation inhibition promotes carbohydrate catabolism and protein deposition through energy homeostasis remodelling. The Journal of Nutrition, nxaa187, https://doi.org/10.1093/jn/nxaa187.en_US
dc.identifier.doihttps://doi.org/10.1093/jn/nxaa187
dc.identifier.urihttp://hdl.handle.net/20.500.11810/5615
dc.publisherOxford University Pressen_US
dc.subjectenergy homeostasis; fatty acid β-oxidation; fish; glucose utilization; insulin sensitivity; protein synthesisen_US
dc.titleMitochondrial fatty acid β-oxidation inhibition promotes carbohydrate catabolism and protein deposition through energy homeostasis remodelling. The Journal of Nutrition, nxaa187, https://doi.org/10.1093/jn/nxaa187.en_US
dc.typeJournal Article, Peer Revieweden_US
Files
Original bundle
Now showing 1 - 1 of 1
Thumbnail Image
Name:
Mitochondrial Fatty Acid β-Oxidation.pdf
Size:
12.13 MB
Format:
Adobe Portable Document Format
Description:
Download
License bundle
Now showing 1 - 1 of 1
No Thumbnail Available
Name:
license.txt
Size:
1.71 KB
Format:
Item-specific license agreed upon to submission
Description:
Download
Collections
Department of Aquaculture Technology