The reduction of lipid-sourced energy production caused by ATGL inhibition cannot be compensated by activation of HSL, autophagy, and utilization of other nutrients in fish. Fish Physiology and Biochemistry, 47: 173–188

Simple item page
dc.contributor.authorSi-Lan Han
dc.contributor.authorYan Liu
dc.contributor.authorSamwel Mchele Limbu
dc.contributor.authorLi-Qiao Chen
dc.contributor.authorMei-Ling Zhang
dc.contributor.authorZhen-Yu Du
dc.date.accessioned2021-04-18T07:21:44Z
dc.date.available2021-04-18T07:21:44Z
dc.date.issued2021-02
dc.description.abstractThe adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL)–mediated lipolysis play important roles in lipid catabolism. ATGL is considered the central rate-limiting enzyme in the mobilization of fatty acids in mammals. Currently, severe fat accumulation has been commonly detected in farmed fish globally. However, the ATGL-mediated lipolysis and the potential synergy among ATGL, HSL, and autophagy, which is another way for lipid breakdown, have not been intensively understood in fish. In the present study, we added Atglistatin as an ATGL-specific inhibitor into the zebrafish diet and fed to the fish for 5 weeks. The results showed that the Atglistatin-treated fish exhibited severe fat deposition, reduced oxygen consumption, and fatty acid β-oxidation, accompanied with increased oxidative stress and inflammation. Furthermore, the Atglistatin-treated fish elevated total and phosphorylation protein expressions of HSL. However, the free fatty acids and lipase activities in organs were still systemically reduced in the Atglistatin-treated fish, and the autophagy marker LC3 was also decreased in the liver. On the other hand, glycogenolysis was stimulated but blood glucose was higher in the Atglistatin-treated fish. The transcriptomic analysis also provided the hint that the protein turnover efficiency in Atglistatin-treated fish was likely to be accelerated, but the protein content in whole fish was not affected. Taken together, ATGL plays crucial roles in energy homeostasis such that its inhibition causes loss of lipid-sourced energy production, which cannot be compensated by activation of HSL, autophagy, and utilization of other nutrients.en_US
dc.description.sponsorshipThe National Natural Science Fund of China (31830102) and the Program of Shanghai Academic Research Leader (19XD1421200)en_US
dc.identifier.citationSi-Lan Han, Yan Liu, Samwel M. Limbu, Li-Qiao Chen, Mei-Ling Zhang and Zhen-Yu Du (2020). The reduction of lipid-sourced energy production caused by ATGL inhibition cannot be compensated by activation of HSL, autophagy, and utilization of other nutrients in fish. Fish Physiology and Biochemistry, 47: 173–188. https://doi.org/10.1007/s10695-020-00904-7.en_US
dc.identifier.doihttps://doi.org/10.1007/s10695-020-00904-7
dc.identifier.urihttp://hdl.handle.net/20.500.11810/5619
dc.publisherSpringeren_US
dc.subjectATGL; Metabolism; Lipolysis; Autophagy;. Energy homeostasis; Zebrafishen_US
dc.titleThe reduction of lipid-sourced energy production caused by ATGL inhibition cannot be compensated by activation of HSL, autophagy, and utilization of other nutrients in fish. Fish Physiology and Biochemistry, 47: 173–188en_US
dc.typeJournal Article, Peer Revieweden_US
Files
Original bundle
Now showing 1 - 1 of 1
Thumbnail Image
Name:
The reduction of lipid-sourced energy production caused.pdf
Size:
3.25 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