Hepatic Hdac3 promotes gluconeogenesis by repressing lipid synthesis and sequestration
Open accessAbstract
Fatty liver disease is associated with obesity and type 2 diabetes, and hepatic lipid accumulation may contribute to insulin resistance. Histone deacetylase 3 (Hdac3) controls the circadian rhythm of hepatic lipogenesis. Here we show that, despite severe hepatosteatosis, mice with liver-specific depletion of Hdac3 have higher insulin sensitivity without any changes in insulin signaling or body weight compared to wild-type mice. Hdac3 depletion reroutes metabolic precursors towards lipid synthesis and storage within lipid droplets and away from hepatic glucose production. Perilipin 2, which coats lipid droplets, is markedly induced upon Hdac3 depletion and contributes to the development of both steatosis and improved tolerance to glucose. These findings suggest that the sequestration of hepatic lipids in perilipin 2–coated droplets ameliorates insulin resistance and establish Hdac3 as a pivotal epigenomic modifier that integrates signals from the circadian clock in the regulation of hepatic intermediary metabolism.
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Mice with a liver-specific deletion of Hdac3 display increased expression of de novo lipogenesis enzymes due to a constitutively active transcriptional environment, resulting in fatty liver disease and elevated serum cholesterol.
“Mice with a liver-specific deletion of Hdac3 display an increased expression of de novo lipogenesis enzymes due to a constitutively active transcriptional environment, resulting in fatty liver disease and elevated serum cholesterol [178,179].”
From Rett syndrome: a neurological disorder with metabolic components (2018) · cites this paper as [179]
The Results sections on Hdac3-depleted fatty liver and metabolic rerouting report that liver-specific Hdac3 deletion increases expression of lipid-synthesis genes and causes hepatosteatosis. The paper describes derepression of lipogenic genes, but does not establish the claimed constitutively active transcriptional environment; no passage found reports elevated serum cholesterol (searched: cholesterol, plasma cholesterol). Page numbers were not available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredLoss of HDAC3 in liver cells leads to metabolic syndrome and FLD.
“its loss in liver cells leads to metabolic syndrome and FLD56,57.”
From A suppressor screen in Mecp2 mutant mice implicates cholesterol metabolism in Rett syndrome (2013) · cites this paper as [56]
The Results sections on hepatic Hdac3 deletion report severe hepatosteatosis in mice, supporting the fatty liver disease (FLD) portion. They do not report that the mice developed metabolic syndrome; instead, the section on glucose output and insulin sensitivity reports lower fasting glucose and insulin and improved insulin sensitivity despite the fatty liver. (LLM, conf=0.90)
Experimental — accuracy not yet measuredHDAC3 regulates lipid homeostasis.
“HDAC3 regulates lipid homeostasis”
From A suppressor screen in Mecp2 mutant mice implicates cholesterol metabolism in Rett syndrome (2013) · cites this paper as [56]
FLD in 129.Mecp2tm1.1Bird mice is similar to that in a liver-specific knockout of HDAC3.
“FLD in 129.Mecp2tm1.1Bird mice is similar to that in a liver-specific knockout of HDAC355,56.”
From A suppressor screen in Mecp2 mutant mice implicates cholesterol metabolism in Rett syndrome (2013) · cites this paper as [56]
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Self-citation
- Authors
- Sun, Z., Miller, R. A., Patel, R. T., Chen, J., Dhir, R., Wang, H., Zhang, D., Graham, M. J., Unterman, T. G., Shulman, G. I., Sztalryd, C., Bennett, M. J., Ahima, R. S., Birnbaum, M. J., & Lazar, M. A.
- Affiliations
- University of Pennsylvania (US)
- Children's Hospital of Philadelphia (US)
- University of Maryland, Baltimore (US)
- Yale University (US)
- Ionis Pharmaceuticals (United States) (US)
- University of Illinois Chicago (US)
- Corresponding author
- Lazar, Mitchell A
- ORCID
- Venue
- Nature Medicine
- Published
- 2012-05-06
- Volume
- 18
- Issue
- 6
- Pages
- 934-942
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC3411870
- OpenAlex
- W2060833045
- Cited by
- 335
- References
- 62
- Citations by year
- 2026: 10 · 2025: 12 · 2024: 25 · 2023: 28 · 2022: 11 · 2021: 24 · 2020: 25 · 2019: 19 · 2018: 27 · 2017: 31 · 2016: 30 · 2015: 30 · 2014: 27 · 2013: 26 · 2012: 9
- FWCI
- 22.03
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (R01-DK40936, R37DK43806, R01DK075017, P01DK049814, P01-DK49210, U24DK059637, R01DK040936, U24DK059635, R01DK056886, P01DK049210, P30DK072488, F32DK079572, R37DK043806, P30DK019525, P30DK050306)
- Topics
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- HDAC3, gluconeogenesis, hepatic insulin resistance, hepatic steatosis, lipid droplets, PLIN2, lipogenesis, circadian clock, type 2 diabetes, glucose tolerance, epigenetic regulation, hepatic metabolism
- MeSH terms
- Histone Deacetylase 3, Animals, Fatty Liver, Gluconeogenesis, Glucose, Histone Deacetylases, Insulin, Insulin Resistance, Lipids, Liver, Male, Mice, Inbred C57BL, Mice, Diet, High-Fat, Non-alcoholic Fatty Liver Disease
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