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Cited by 102Lipid metabolism and biosynthesisLiver Disease Diagnosis and TreatmentCancer, Lipids, and Metabolism

DGAT2 inhibition blocks SREBP-1 cleavage and improves hepatic steatosis by increasing phosphatidylethanolamine in the ER

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Rong, Shunxing, Xia, Mingfeng, Vale, Goncalo, Wang, Simeng, Kim, Chai-Wan, Li, Shili, McDonald, Jeffrey G., Radhakrishnan, Arun +1 more·2024·Cell Metabolism
DOI 10.1016/j.cmet.2024.01.011PMC PMC10939742
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Abstract

Diacylglycerol acyltransferase 2 (DGAT2) catalyzes the final step of triglyceride (TG) synthesis. DGAT2 deletion in mice lowers liver TGs, and DGAT2 inhibitors are under investigation for the treatment of fatty liver disease. Here, we show that DGAT2 inhibition also suppressed SREBP-1 cleavage, reduced fatty acid synthesis, and lowered TG accumulation and secretion from liver. DGAT2 inhibition increased phosphatidylethanolamine (PE) levels in the endoplasmic reticulum (ER) and inhibited SREBP-1 cleavage, while DGAT2 overexpression lowered ER PE concentrations and increased SREBP-1 cleavage in vivo. ER enrichment with PE blocked SREBP-1 cleavage independent of Insigs, which are ER proteins that normally retain SREBPs in the ER. Thus, inhibition of DGAT2 shunted diacylglycerol into phospholipid synthesis, increasing the PE content of the ER, resulting in reduced SREBP-1 cleavage and less hepatic steatosis. This study reveals a new mechanism that regulates SREBP-1 activation and lipogenesis that is independent of sterols and SREBP-2 in liver.

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  • Liver studies showed that inhibition of DGAT2 does not result in excessive FFA accumulation, because the resulting increase of available DGs leads to reduction of de novo lipogenesis through suppression of SREBP-1.

    “Importantly, liver studies showed that inhibition of DGAT2 does not result in excessive FFA accumulation, because the resulting increase of available DGs leads to reduction of de novo lipogenesis through suppression of SREBP-1 –a regulator of fatty acid synthesis.84”

    From Amyloid-β induces lipid droplet-mediated microglial dysfunction via the enzyme DGAT2 in Alzheimer’s disease (2025) · cites this paper as [84]

    The Results and Discussion report that DGAT2 inhibition redirects diacylglycerols toward phosphatidylethanolamine synthesis, suppresses SREBP-1 cleavage, and reduces hepatic de novo lipogenesis. Our copy does not report whether free fatty acids accumulate excessively, so that part of the claim is unsupported. Page numbers were not available in the indexed passages. (LLM, conf=0.87)

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Cited by

Sorted by citations

Authors
Rong, S., Xia, M., Vale, G., Wang, S., Kim, C.-W., Li, S., McDonald, J. G., Radhakrishnan, A., & Horton, J. D.
Affiliations
  • The University of Texas Southwestern Medical Center (US)
  • Fudan University (CN)
Corresponding author
Horton, Jay D.
ORCID
Venue
Cell Metabolism
Publisher
Elsevier BV
Published
2024-03
Volume
36
Issue
3
Pages
617-629.e7
ISSN
1550-4131 (ISSN-L)
DOI
10.1016/j.cmet.2024.01.011
PMC
PMC10939742
OpenAlex
W4391692569
Cited by
102
References
11
Citations by year
2026: 37 · 2025: 50 · 2024: 15
FWCI
16.38
Type
journal article
Language
en
Open access
Licence
Locations
  • Cell Metabolism (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion, cc-by-nc)
Funders
  • Leducq Foundation (19CVD04)
  • Welch Foundation (I-1793)
  • Science and Technology Commission of Shanghai Municipality (23ZR1411000)
  • Merck
  • Pfizer
  • NIH (P30DK127984, UL1TR003163, P01HL-160487, AI-158357)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
  • Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
Keywords
hepatic steatosis, phosphatidylethanolamine, endoplasmic reticulum, fatty acid synthesis, triglyceride synthesis, lipogenesis, diacylglycerol, SREBP
MeSH terms
Animals, Endoplasmic Reticulum, Liver, Phosphatidylethanolamines, Triglycerides, Diacylglycerol O-Acyltransferase, Mice, Sterol Regulatory Element Binding Protein 1, Non-alcoholic Fatty Liver Disease

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