Disruption of Hepatic Adipogenesis Is Associated With Impaired Liver Regeneration in Mice
Open accessAbstract
The liver responds to injury with regulated tissue regeneration. During early regeneration, the liver accumulates fat. Neither the mechanisms responsible for nor the functional significance of this transient steatosis have been determined. In this study, we examined patterns of gene expression associated with hepatic fat accumulation in regenerating liver and tested the hypothesis that disruption of hepatic fat accumulation would be associated with impaired hepatic regeneration. First, microarray–based gene expression analysis revealed that several genes typically induced during adipocyte differentiation were specifically upregulated in the regenerating liver prior to peak hepatocellular fat accumulation. These observations suggest that hepatic fat accumulation is specifically regulated during liver regeneration. Next, 2 methods were employed to disrupt hepatocellular fat accumulation in the regenerating liver. Because exogenous leptin supplementation reverses hepatic steatosis in leptin–deficient mice, the effects of leptin supplementation on liver regeneration in wild–type mice were examined. The data showed that leptin supplementation resulted in suppression of hepatocellular fat accumulation and impairment of hepatocellular proliferation during liver regeneration. Second, because glucocorticoids regulate cellular fat accumulation during adipocyte differentiation, the effects of hepatocyte–specific disruption of the glucocorticoid receptor were similarly evaluated. The results showed that hepatic fat accumulation and hepatocellular proliferation were also suppressed in mice with liver specific disruption of glucocorticoid receptor. In conclusion , suppression of hepatocellular fat accumulation is associated with impaired hepatocellular proliferation following partial hepatectomy, indicating that hepatocellular fat accumulation is specifically regulated during and may be essential for normal liver regeneration. (Hepatology 2004;40:1322-1332.)
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Transient hypoglycemia, hepatic steatosis, and BA overload occur after PHx.
“Consistent with prior reports of transient hypoglycemia,34,35 hepatic steatosis,34,53 and BA overload4,34 occurring after PHx”
From Constitutive Androstane Receptor Regulates Bile Acid Homeostasis and Metabolism During Liver Regeneration (2026) · cites this paper as [53]
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Analysis of the role of hepatic PPARγ expression during mouse liver regeneration
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- Authors
- Shteyer, E., Liao, Y., Muglia, L. J., Hruz, P. W., & Rudnick, D. A.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Rudnick, David A.
- Venue
- Hepatology
- Published
- 2004-12
- Volume
- 40
- Issue
- 6
- Pages
- 1322-1332
- ISSN
- 0270-9139 (ISSN-L)
- OpenAlex
- W2013853905
- Cited by
- 234
- References
- 53
- Citations by year
- 2026: 8 · 2025: 7 · 2024: 7 · 2023: 12 · 2022: 13 · 2021: 12 · 2020: 13 · 2019: 9 · 2018: 14 · 2017: 11 · 2016: 12 · 2015: 11 · 2014: 4 · 2013: 14 · 2012: 18
- FWCI
- 5.61
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Hepatology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Alvin J. Siteman Cancer Center
- National Institutes of Health (1p30hd033688-01, 1r03dk064653-01, DK064572)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30 DK-52574, DK-02900, DK64653, R01DK064572, DK-064572, K08DK002900, P30DK052574)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD 33688)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Surgery › Tissue Engineering and Regenerative Medicine
- Keywords
- liver regeneration, hepatic steatosis, leptin, glucocorticoid receptor, hepatocyte proliferation, partial hepatectomy, gene expression, ob/ob mice
- MeSH terms
- Animals, Cell Division, Fats, Hepatectomy, Liver, Liver Regeneration, Male, Mice, Inbred C57BL, Receptors, Glucocorticoid, Oligonucleotide Array Sequence Analysis, Leptin, Hepatocytes, Mice
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