SIRT3-mediated mitochondrial fatty acid oxidation protects against hepatic lipid deposition in fatty liver hemorrhagic syndrome.

Λεπτομέρειες βιβλιογραφικής εγγραφής
Τίτλος: SIRT3-mediated mitochondrial fatty acid oxidation protects against hepatic lipid deposition in fatty liver hemorrhagic syndrome.
Συγγραφείς: Cao P; Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang 330045, Jiangxi, PR China., Chen J; Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang 330045, Jiangxi, PR China., Zeng C; Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang 330045, Jiangxi, PR China., Hu Y; College of Computer and Information Engineering, Jiangxi Agricultural University, Nanchang 330045, Jiangxi, PR China., Yuan J; Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang 330045, Jiangxi, PR China., Guo X; Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang 330045, Jiangxi, PR China., Cao H; Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang 330045, Jiangxi, PR China., Zhang C; Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang 330045, Jiangxi, PR China., Zhuang Y; Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang 330045, Jiangxi, PR China., Hu G; Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang 330045, Jiangxi, PR China. Electronic address: hgljx3818@jxau.edu.cn.
Πηγή: Poultry science [Poult Sci] 2026 Jul; Vol. 105 (7), pp. 106901. Date of Electronic Publication: 2026 Apr 07.
Τύπος έκδοσης: Journal Article
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: Elsevier Country of Publication: England NLM ID: 0401150 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1525-3171 (Electronic) Linking ISSN: 00325791 NLM ISO Abbreviation: Poult Sci Subsets: MEDLINE
Imprint Name(s): Publication: 2020- : [Cambridge, UK] : Elsevier
Original Publication: Champaign Il : Poultry Science Association
Ιατρικοί όροι (MeSH): Sirtuin 3*/metabolism , Sirtuin 3*/genetics , Fatty Liver*/veterinary , Fatty Liver*/metabolism , Fatty Acids*/metabolism , Poultry Diseases*/metabolism , Avian Proteins*/metabolism , Avian Proteins*/genetics , Chickens* , Lipid Metabolism*, Liver/metabolism ; Diet/veterinary ; Hepatocytes/metabolism ; Mitochondria/metabolism ; Animals ; Oxidation-Reduction ; Female
Περίληψη: Fatty liver hemorrhagic syndrome (FLHS) is a nutrition-related metabolic disorder in laying hens characterized by excessive hepatic lipid accumulation and hemorrhagic lesions, leading to reduced productivity and increased mortality. However, the regulatory mechanisms linking mitochondrial dysfunction to hepatic lipid metabolism remain unclear. This study investigated the role of SIRT3 in modulating mitochondrial fatty acid oxidation during FLHS progression. An in vivo FLHS model was established by feeding laying hens with a high-energy, low-protein (HELP) diet, and an in vitro hepatic steatosis model was induced by free fatty acid (FFA) treatment in primary hepatocytes. Both models exhibited pronounced lipid accumulation in hepatic cells and altered hepatocellular injury-related parameters, which were associated with mitochondrial dysfunction and impaired fatty acid oxidation. Mechanistically, hepatic tissues and hepatocytes showed suppression of the SIRT3-AMPKα-PGC-1α signaling cascade, accompanied by reduced expression of mitochondrial biogenesis markers (NRF1, TFAM), impaired respiratory chain components (NDUFA9, SDHA, UQCRC1, COX4I1, ATP5B), and decreased transcription of fatty acid oxidation-related genes (PPARα, ACOX1, CPT1A, CPT2, ACADL, ACADM). Pharmacological activation of SIRT3 with AR-C17 restored AMPKα-PGC-1α signaling, enhanced mitochondrial biogenesis and respiratory function, and promoted fatty acid oxidation, thereby alleviating lipid accumulation in hepatocytes in both models. Collectively, these results demonstrate that SIRT3 is a key metabolic regulator maintaining mitochondrial oxidative function and lipid homeostasis in laying hens. Targeted activation of SIRT3 may provide a novel nutritional strategy for preventing or ameliorating FLHS and related metabolic disturbances in poultry production.
(Copyright © 2026. Published by Elsevier Inc.)
Competing Interests: Disclosures The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Contributed Indexing: Keywords: Fatty acid oxidation; Fatty liver hemorrhagic syndrome; Mitochondrial biogenesis; SIRT3
Substance Nomenclature: EC 3.5.1.- (Sirtuin 3)
0 (Fatty Acids)
0 (Avian Proteins)
Entry Date(s): Date Created: 20260412 Date Completed: 20260616 Latest Revision: 20260616
Update Code: 20260616
PubMed Central ID: PMC13091748
DOI: 10.1016/j.psj.2026.106901
PMID: 41967321
Βάση Δεδομένων: MEDLINE
Περιγραφή
ISSN:1525-3171
DOI:10.1016/j.psj.2026.106901