ArticleThe Journal of endocrinology2017
Hepatocyte-specific, PPARγ-regulated mechanisms to promote steatosis in adult mice.
Article in The Journal of endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 75 citations in OpenAlex.
- Hepatocyte-specific PPARγ Deletion Uncovers Role of an Antagonistic PPARγ-HNF4α Transcriptional Axis in Metabolic Dysfunction-Associated Steatotic Liver Disease Progression.The American journal of pathology · 2026Article
- Loss of peroxisomal membrane proteins PEX13 and PEX14 disrupts fatty acid oxidation and drives lipid imbalance.Bioscience reports · 2026Article
- PPARγ-dependent and -independent regulation of methionine metabolism by diet-induced obesity and fasting in male mice.bioRxiv : the preprint server for biology · 2026Article
- Sex- and hepatocyte PPARbioRxiv : the preprint server for biology · 2026Article
- PPARγ-dependent and -independent regulation of genes involved in hepatic methionine cycle in fasted or diet-induced obese mice.PloS one · 2026Article
- Unlocking the benefits of aerobic exercise for MAFLD: a comprehensive mechanistic analysis.Journal of translational medicine · 2025Review
- Hepatocellular EVs Regulate Lipid Metabolism via SIRT1/SREBP-1c/PGC-1α Signaling in Primary Calf Hepatocytes.International journal of molecular sciences · 2025Article
- Static magnetic field exposure modulates gut microbiota and host metabolism to alleviate high-fat diet-induced metabolic dysfunction-associated fatty liver disease.Zoological research · 2025Article
- Exploring the prognostic value of the novel nutritional index for in-hospital mortality in acute coronary syndrome: a sex-specific analysis.Frontiers in medicine · 2025Article
- Gallic acid mitigates high-fat and high-carbohydrate diet-induced steatohepatitis by modulating the IRF6/PPARγ signaling pathway.Frontiers in pharmacology · 2025Article
- Dietary Influences on Gut Microbiota and Their Role in Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD).Nutrients · 2024Review
- The Influence of the FFAR4 Agonist TUG-891 on Liver Steatosis in ApoE-Knockout Mice.Cardiovascular drugs and therapy · 2024Article
- Article
- Direct and systemic actions of growth hormone receptor (GHR)-signaling on hepatic glycolysis, de novo lipogenesis and insulin sensitivity, associated with steatosis.Metabolism: clinical and experimental · 2023Article
- miR-27b targets MAIP1 to mediate lipid accumulation in cultured human and mouse hepatic cells.Communications biology · 2023Article
- Liver insulin-like growth factor-1 mediates effects of low-intensity vibration on wound healing in diabetic mice.The Journal of pathology · 2023Article
- Role of hepatic peroxisome proliferator-activated receptor γ in non-alcoholic fatty liver disease.The Journal of endocrinology · 2023Review
- Metabolism-Disrupting Chemicals Affecting the Liver: Screening, Testing, and Molecular Pathway Identification.International journal of molecular sciences · 2023Review
- Hepatocyte PPARγ contributes to the progression of non-alcoholic steatohepatitis in male and female obese mice.Cellular and molecular life sciences : CMLS · 2023Article
- Hepatic transcriptome profiling reveals early signatures associated with disease transition from non-alcoholic steatosis to steatohepatitis.Liver research (Beijing, China) · 2022Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Peroxisome proliferator-activated receptor γ (PPARγ) is the target for thiazolidinones (TZDs), drugs that improve insulin sensitivity and fatty liver in humans and rodent models, related to a reduction in hepatic de novo lipogenesis (DNL). The systemic effects of TZDs are in contrast to reports suggesting hepatocyte-specific activation of PPARγ promotes DNL, triacylglycerol (TAG) uptake and fatty acid (FA) esterification. As these hepatocyte-specific effects of PPARγ could counterbalance the positive therapeutic actions of systemic delivery of TZDs, the current study used a mouse model of adult-onset, liver (hepatocyte)-specific PPARγ knockdown (aLivPPARγkd). This model has advantages over existing congenital knockout models, by avoiding compensatory changes related to embryonic knockdown, thus better modeling the impact of altering PPARγ on adult physiology, where metabolic diseases most frequently develop. The impact of aLivPPARγkd on hepatic gene expression and endpoints in lipid metabolism was examined after 1 or 18 weeks (Chow-fed) or after 14 weeks of low- or high-fat (HF) diet. aLivPPARγkd reduced hepatic TAG content but did not impact endpoints in DNL or TAG uptake. However, aLivPPARγkd reduced the expression of the FA translocase (Cd36), in 18-week Chow- and HF-fed mice, associated with increased NEFA after HF feeding. Also, aLivPPARγkd dramatically reduced Mogat1 expression, that was reflected by an increase in hepatic monoacylglycerol (MAG) levels, indicative of reduced MOGAT activity. These results, coupled with previous reports, suggest that Cd36-mediated FA uptake and MAG pathway-mediated FA esterification are major targets of hepatocyte PPARγ, where loss of this control explains in part the protection against steatosis observed after aLivPPARγkd.
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