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Peer-reviewedCC BYFASEB bioAdvances

Hepatic Overexpression of Lysophospholipid Acyltransferase LPLAT14/MBOAT1 Ameliorates Mild Liver Injury During Early High‐Fat Diet Feeding

  • Sho Hori1
  • Kahori Shimizu1,2
  • Taiga Kikuchi2
  • Hajime Miyata2
  • Hiroaki Hase1,2
  • Hiroki Nakanishi3
  • Hideo Shindou4,5
  • Hiroyuki Mizuguchi1,2,6,7,8
8 affiliations
  1. 1Laboratory of Biochemistry and Molecular Biology, Graduate School of Pharmaceutical Sciences The University of Osaka Osaka Japan
  2. 2Laboratory of Biochemistry and Molecular Biology, School of Pharmaceutical Sciences The University of Osaka Osaka Japan
  3. 3Lipidome Lab Co., Ltd. Akita Japan
  4. 4Department of Lipid Life Science, National Institute of Global Health and Medicine Japan Institute for Health Security Tokyo Japan
  5. 5Department of Medical Lipid Science, Graduate School of Medicine The University of Tokyo Tokyo Japan
  6. 6Global Center for Medical Engineering and Informatics The University of Osaka Osaka Japan
  7. 7Integrated Frontier Research for Medical Science Division, Institute for Open and Transdisciplinary Research Initiatives The University of Osaka Osaka Japan
  8. 8Center for Infectious Disease Education and Research The University of Osaka Osaka Japan
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Abstract

Metabolic dysfunction‐associated steatotic liver disease (MASLD) encompasses a spectrum of conditions progressing from simple steatosis to severe steatohepatitis. During this progression, liver injury associated with lipotoxicity and altered membrane phospholipid homeostasis is thought to contribute to disease aggravation. Although lysophospholipid acyltransferases (LPLATs) regulate membrane lipid remodeling and contribute to cellular integrity, the physiological roles of several LPLATs have only partially been characterized, and the in vivo functions of LPLAT14 remain largely unknown. Here, we investigated the effects of hepatic overexpression of LPLAT14 on high‐fat diet (HFD)‐induced metabolic disorders and mild liver injury in mice using an improved adenovirus (Ad) vector. Hepatic LPLAT14 overexpression did not significantly alter body weight, systemic glucose tolerance, or hepatic lipid accumulation. Targeted lipidomics revealed that LPLAT14 overexpression selectively significantly increased oleic acid (OA)‐containing phosphatidylserine (PS) species in the liver, suggesting selective incorporation of OA into lysophosphatidylserine. This specific lipidomic remodeling significantly attenuated mild liver injury during early HFD feeding, as evidenced by reduced serum alanine aminotransferase levels at 2 weeks after Ad‐LPLAT14 treatment. However, this hepatoprotective effect was not observed in the later phase (8 weeks), when severe lipid accumulation had developed, suggesting that LPLAT14 primarily attenuates mild liver injury during early HFD feeding. Collectively, our findings suggest that LPLAT14‐mediated enrichment of OA‐containing PS attenuates mild liver injury during early HFD feeding, possibly through protection against early cellular stress.

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Cite

BibTeXRIS
BibTeX
@article{hori2026hepatic,
  title = {{Hepatic Overexpression of Lysophospholipid Acyltransferase LPLAT14/MBOAT1 Ameliorates Mild Liver Injury During Early High‐Fat Diet Feeding}},
  author = {Sho Hori and Kahori Shimizu and Taiga Kikuchi and Hajime Miyata and Hiroaki Hase and Hiroki Nakanishi and Hideo Shindou and Hiroyuki Mizuguchi},
  journal = {FASEB bioAdvances},
  year = {2026},
  month = nov,
  doi = {10.1096/fba.2026-00165},
  url = {https://europepmc.org/article/PMC/PMC13725374},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Hepatic Overexpression of Lysophospholipid Acyltransferase LPLAT14/MBOAT1 Ameliorates Mild Liver Injury During Early High‐Fat Diet Feeding
AU  - Sho Hori
AU  - Kahori Shimizu
AU  - Taiga Kikuchi
AU  - Hajime Miyata
AU  - Hiroaki Hase
AU  - Hiroki Nakanishi
AU  - Hideo Shindou
AU  - Hiroyuki Mizuguchi
PY  - 2026
DA  - 2026/11/01
JO  - FASEB bioAdvances
DO  - 10.1096/fba.2026-00165
UR  - https://europepmc.org/article/PMC/PMC13725374
AB  - Metabolic dysfunction‐associated steatotic liver disease (MASLD) encompasses a spectrum of conditions progressing from simple steatosis to severe steatohepatitis. During this progression, liver injury associated with lipotoxicity and altered membrane phospholipid homeostasis is thought to contribute to disease aggravation. Although lysophospholipid acyltransferases (LPLATs) regulate membrane lipid remodeling and contribute to cellular integrity, the physiological roles of several LPLATs have only partially been characterized, and the in vivo functions of LPLAT14 remain largely unknown. Here, we investigated the effects of hepatic overexpression of LPLAT14 on high‐fat diet (HFD)‐induced metabolic disorders and mild liver injury in mice using an improved adenovirus (Ad) vector. Hepatic LPLAT14 overexpression did not significantly alter body weight, systemic glucose tolerance, or hepatic lipid accumulation. Targeted lipidomics revealed that LPLAT14 overexpression selectively significantly increased oleic acid (OA)‐containing phosphatidylserine (PS) species in the liver, suggesting selective incorporation of OA into lysophosphatidylserine. This specific lipidomic remodeling significantly attenuated mild liver injury during early HFD feeding, as evidenced by reduced serum alanine aminotransferase levels at 2 weeks after Ad‐LPLAT14 treatment. However, this hepatoprotective effect was not observed in the later phase (8 weeks), when severe lipid accumulation had developed, suggesting that LPLAT14 primarily attenuates mild liver injury during early HFD feeding. Collectively, our findings suggest that LPLAT14‐mediated enrichment of OA‐containing PS attenuates mild liver injury during early HFD feeding, possibly through protection against early cellular stress.
SN  - 2573-9832
ER  -