ArticleHepatology (Baltimore, Md.)2019
Hepatocyte Deletion of Triglyceride-Synthesis Enzyme Acyl CoA: Diacylglycerol Acyltransferase 2 Reduces Steatosis Without Increasing Inflammation or Fibrosis in Mice.
Article in Hepatology (Baltimore, Md.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
74 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.
- Key hepatic signatures of human and mouse nonalcoholic steatohepatitis: A transcriptome-proteome data meta-analysis.Frontiers in endocrinology · 2022Pooled it
- ACC inhibitor alone or co-administered with a DGAT2 inhibitor in patients with non-alcoholic fatty liver disease: two parallel, placebo-controlled, randomized phase 2a trials.Nature medicine · 2021Trial
- Global deletion of the triglyceride-synthesizing enzyme TMEM68 disrupts hepatic lipid homeostasis in mice.Journal of physiology and biochemistry · 2026Article
- Local Suppression ofJournal of microbiology and biotechnology · 2026Article
- Deletion of Pleiotrophin protects against high-fat diet-induced liver metabolic disease, independently of the sexual dimorphism in dietary response.Molecular biomedicine · 2026Article
- Hepatic SEC16B regulates lipid homeostasis by coordinating VLDL secretion and lipid droplet expansion.The Journal of clinical investigation · 2026Article
- Fucoxanthin Suppresses Lipid Accumulation and Inflammatory Responses in FFA-Induced Hepatocyte Models via the EGR2-CD36 Axis.Molecules (Basel, Switzerland) · 2026Article
- A membrane homeostatic response to lipid overload coordinates fatty acid metabolism.bioRxiv : the preprint server for biology · 2026Article
- [EVA1A overexpression improves non-alcoholic fatty liver disease in mice by regulating lipid metabolism and promoting lipophagy].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Interorganelle competition for linoleic acid underlies steatotic liver pathology.bioRxiv : the preprint server for biology · 2026Article
- Transcriptomic Changes Underlying the Anti-Steatotic Effects of DHA Supplementation in Aged Obese Female Mice.International journal of molecular sciences · 2025Article
- Polymer-lipid hybrid nanoparticles incorporating green coffee extract: enhancing treatment for hepatic steatosis and fibrosis through metabolomic insights.RSC advances · 2025Article
- miR-10c TargetsInternational journal of molecular sciences · 2025Article
- CES1 Increases Hepatic Triacylglycerol Synthesis Through Activation of PPARγ, LXR and SREBP1c.Cells · 2025Article
- MASH: the nexus of metabolism, inflammation, and fibrosis.The Journal of clinical investigation · 2025Review
- The pathogenesis of hepatic steatosis in MASLD: a lipid droplet perspective.The Journal of clinical investigation · 2025Article
- Essential Biology of Lipid Droplets.Annual review of biochemistry · 2025Review
- Hepatocyte-specific CLSTN3B ablation impairs lipid droplet maturation and alleviates diet-induced steatohepatitis in mice.bioRxiv : the preprint server for biology · 2025Article
- Silybin A fromTheranostics · 2025Article
- Synergistic therapeutic strategies for metabolic dysfunction-associated steatohepatitis and type 2 diabetes mellitus: molecular insights and clinical advances.Frontiers in endocrinology · 2025Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Nonalcoholic fatty liver disease (NAFLD) is characterized by excess lipid accumulation in hepatocytes and represents a huge public health problem owing to its propensity to progress to nonalcoholic steatohepatitis, fibrosis, and liver failure. The lipids stored in hepatic steatosis (HS) are primarily triglycerides (TGs) synthesized by two acyl-CoA:diacylglycerol acyltransferase (DGAT) enzymes. Either DGAT1 or DGAT2 catalyzes this reaction, and these enzymes have been suggested to differentially utilize exogenous or endogenously synthesized fatty acids, respectively. DGAT2 has been linked to storage of fatty acids from de novo lipogenesis, a process increased in NAFLD. However, whether DGAT2 is more responsible for lipid accumulation in NAFLD and progression to fibrosis is currently unknown. Also, it is unresolved whether DGAT2 can be safely inhibited as a therapy for NAFLD. Here, we induced NAFLD-like disease in mice by feeding a diet rich in fructose, saturated fat, and cholesterol and found that hepatocyte-specific Dgat2 deficiency reduced expression of de novo lipogenesis genes and lowered liver TGs by ~70%. Importantly, the reduction in steatosis was not accompanied by increased inflammation or fibrosis, and insulin and glucose metabolism were unchanged. Conclusion: This study suggests that hepatic DGAT2 deficiency successfully reduces diet-induced HS and supports development of DGAT2 inhibitors as a therapeutic strategy for treating NAFLD and preventing downstream consequences.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.