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Transcriptional regulation of hepatic lipogenesis
Open accessAbstract
Fatty acid and fat synthesis in the liver is a highly regulated metabolic pathway that is important for very low-density lipoprotein (VLDL) production and thus energy distribution to other tissues. Having common features at their promoter regions, lipogenic genes are coordinately regulated at the transcriptional level. Transcription factors, such as upstream stimulatory factors (USFs), sterol regulatory element-binding protein 1C (SREBP1C), liver X receptors (LXRs) and carbohydrate-responsive element-binding protein (ChREBP) have crucial roles in this process. Recently, insights have been gained into the signalling pathways that regulate these transcription factors. After feeding, high blood glucose and insulin levels activate lipogenic genes through several pathways, including the DNA-dependent protein kinase (DNA-PK), atypical protein kinase C (aPKC) and AKT-mTOR pathways. These pathways control the post-translational modifications of transcription factors and co-regulators, such as phosphorylation, acetylation or ubiquitylation, that affect their function, stability and/or localization. Dysregulation of lipogenesis can contribute to hepatosteatosis, which is associated with obesity and insulin resistance.
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In the citing paper
“ChREBP, which is a member of the Mondo family of transcription factors, senses carbohydrates and activates genes involved in glycolysis, DNL, and lipid trafficking [2,34,78].”
From Hepatic Insulin Resistance and Steatosis in Metabolic Dysfunction-Associated Steatotic Liver Disease: New Insights into Mechanisms and Clinical Implications (2025) · cites this paper as [34]
In the citing paper
“DNL is minimal during fasting but increases after a meal as glucose and insulin levels rise, activating insulin signaling via PI3K, AKT, aPKC, mTORC, DNA-dependent protein kinase, and phosphatases [34,83].”
From Hepatic Insulin Resistance and Steatosis in Metabolic Dysfunction-Associated Steatotic Liver Disease: New Insights into Mechanisms and Clinical Implications (2025) · cites this paper as [34]
In the citing paper
“However, it decreased in the presence of severe IR [34,94].”
From Hepatic Insulin Resistance and Steatosis in Metabolic Dysfunction-Associated Steatotic Liver Disease: New Insights into Mechanisms and Clinical Implications (2025) · cites this paper as [34]
In the citing paper
“This result also demonstrates that hepatic steatosis is not necessarily accompanied by IR in DNL in the liver and can be initiated by factors other than insulin signaling [34].”
From Hepatic Insulin Resistance and Steatosis in Metabolic Dysfunction-Associated Steatotic Liver Disease: New Insights into Mechanisms and Clinical Implications (2025) · cites this paper as [34]
In the citing paper
“Thus, insulin activates specific kinases and phosphatases that can modify transcription factors such as upstream stimulatory factor (USF), SREBP1c, ChREBP, and liver X receptor (LXR), or regulate the expression of these transcription factors (Fig. 4) [34,83].”
From Hepatic Insulin Resistance and Steatosis in Metabolic Dysfunction-Associated Steatotic Liver Disease: New Insights into Mechanisms and Clinical Implications (2025) · cites this paper as [34]
In the citing paper
“ChREBP, which is activated by carbohydrate uptake [9,34,78,83].”
From Hepatic Insulin Resistance and Steatosis in Metabolic Dysfunction-Associated Steatotic Liver Disease: New Insights into Mechanisms and Clinical Implications (2025) · cites this paper as [34]
In the citing paper
“In this regard, ChREBP expression in liver biopsies from patients with MASH was observed to be two-fold higher when the histologic steatosis score was greater than 50% compared to those with less than 50%.”
From Hepatic Insulin Resistance and Steatosis in Metabolic Dysfunction-Associated Steatotic Liver Disease: New Insights into Mechanisms and Clinical Implications (2025) · cites this paper as [34]
In the citing paper
“Supporting this perspective, monosaccharides have been shown to activate ChREBP and other key lipogenic transcription factors—including SREBP1c, LXR, and PPARγ—via insulin-independent mechanisms [34,70,83,86,99].”
From Hepatic Insulin Resistance and Steatosis in Metabolic Dysfunction-Associated Steatotic Liver Disease: New Insights into Mechanisms and Clinical Implications (2025) · cites this paper as [34]
In the citing paper
“Additionally, substrate-driven pathways as insulin-independent mechanisms contribute to elevated DNL and enhanced esterification of FFAs into hepatic TG [34,70,85,86].”
From Hepatic Insulin Resistance and Steatosis in Metabolic Dysfunction-Associated Steatotic Liver Disease: New Insights into Mechanisms and Clinical Implications (2025) · cites this paper as [34]
In the citing paper
“VLDL assembly and secretion are upregulated by (i) the delivery of FA released from insulin-resistant adipocytes, (ii) the increased delivery of remnant TG–FA to the liver due to reduced peripheral lipolysis of chylomicron and VLDL–TG, and (iii) the increased de novo lipogenesis55 (Figure 4).”
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Metadata
- Authors
- Wang, Y., Viscarra, J., Kim, S.-J., & Sul, H. S.
- Affiliations
- University of California, Berkeley (US)
- Corresponding author
- Sul, Hei Sook
- Venue
- Nature Reviews Molecular Cell Biology
- Published
- 2015-10-22
- Volume
- 16
- Issue
- 11
- Pages
- 678-689
- ISSN
- 1471-0072 (ISSN-L)
- 1471-0080
- PMC
- PMC4884795
- OpenAlex
- W2174107467
- Cited by
- 646
- References
- 135
- Citations by year
- 2026: 24 · 2025: 52 · 2024: 60 · 2023: 71 · 2022: 85 · 2021: 74 · 2020: 84 · 2019: 62 · 2018: 67 · 2017: 49 · 2016: 17 · 2015: 1
- FWCI
- 4.23
- Type
- journal article
- Language
- en
- Update notices
- erratum (2015-12-16)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Reviews Molecular Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK105671, F32DK105671, R01DK081098, DK081098)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Keywords
- hepatic lipogenesis, transcriptional regulation, upstream stimulatory factor, SREBP-1c, liver X receptor, ChREBP, DNA-dependent protein kinase, atypical protein kinase C, Akt/mTOR signaling, VLDL production, hepatic steatosis, insulin resistance, obesity
- MeSH terms
- Liver X Receptors, Animals, Fatty Acids, Gene Expression Regulation, Lipoproteins, VLDL, Liver, Nuclear Proteins, Protein Kinase C, Protein Processing, Post-Translational, Transcription Factors, Transcription, Genetic, Signal Transduction, Lipogenesis, Proto-Oncogene Proteins c-akt, Mice, Upstream Stimulatory Factors, DNA-Activated Protein Kinase, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Sterol Regulatory Element Binding Protein 1, Orphan Nuclear Receptors, TOR Serine-Threonine Kinases
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