ArticleJournal of lipid research2015
Liver X receptor regulates hepatic nuclear O-GlcNAc signaling and carbohydrate responsive element-binding protein activity.
Article in Journal of lipid research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
38 citing papers in PubMed, 62 citations in OpenAlex.
- Review
- Emerging Roles of Post-Translational Modifications in Metabolic Homeostasis and Type 2 Diabetes.International journal of molecular sciences · 2025Review
- Protein O-GlcNAcylation in reproductive biology and the impact of metabolic disease.Human reproduction update · 2025Review
- Adropin: a key player in immune cell homeostasis and regulation of inflammation in several diseases.Frontiers in immunology · 2025Review
- A 40-year challenge to resolve clinical questions through experimental/laboratory techniques.Endocrine journal · 2025Article
- Unveiling the multifaceted role of adropin in various diseases (Review).International journal of molecular medicine · 2024Review
- LXR-dependent enhancer activation regulates the temporal organization of the liver's response to refeeding leading to lipogenic gene overshoot.PLoS biology · 2024Article
- Metabolic Dysfunction-Associated Steatotic Liver Disease: From Pathogenesis to Current Therapeutic Options.International journal of molecular sciences · 2024Review
- Review
- Changes in Cells Associated with Insulin Resistance.International journal of molecular sciences · 2024Review
- In-depth analysis ofLiver research (Beijing, China) · 2023Review
- Metabolic dysfunction-associated fatty liver disease (MAFLD): an update of the recent advances in pharmacological treatment.Journal of physiology and biochemistry · 2023Review
- Insulin Regulation of Hepatic Lipid Homeostasis.Comprehensive Physiology · 2023Review
- Emerging Role of Protein O-GlcNAcylation in Liver Metabolism: Implications for Diabetes and NAFLD.International journal of molecular sciences · 2023Review
- Lipidomic and Membrane Mechanical Signatures in Triple-Negative Breast Cancer: Scope for Membrane-Based Theranostics.Molecular and cellular biochemistry · 2022Review
- Regulation of the urea cycle by CPS1 O-GlcNAcylation in response to dietary restriction and aging.Journal of molecular cell biology · 2022Article
- Nutrition, metabolism, and epigenetics: pathways of circadian reprogramming.EMBO reports · 2022Review
- A nexus of lipid andFrontiers in endocrinology · 2022Review
- Insulin Resistance: From Mechanisms to Therapeutic Strategies.Diabetes & metabolism journal · 2022Review
- How cancer cells remodel lipid metabolism: strategies targeting transcription factors.Lipids in health and disease · 2021Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 5 countries.
Funding
Abstract
Liver X receptor (LXR)α and LXRβ play key roles in hepatic de novo lipogenesis through their regulation of lipogenic genes, including sterol regulatory element-binding protein (SREBP)-1c and carbohydrate responsive element-binding protein (ChREBP). LXRs activate lipogenic gene transcription in response to feeding, which is believed to be mediated by insulin. We have previously shown that LXRs are targets for glucose-hexosamine-derived O-linked β-N-acetylglucosamine (O-GlcNAc) modification enhancing their ability to regulate SREBP-1c promoter activity in vitro. To elucidate insulin-independent effects of feeding on LXR-mediated lipogenic gene expression in vivo, we subjected control and streptozotocin-treated LXRα/β(+/+) and LXRα/β(-/-) mice to a fasting-refeeding regime. We show that under hyperglycemic and hypoinsulinemic conditions, LXRs maintain their ability to upregulate the expression of glycolytic and lipogenic enzymes, including glucokinase (GK), SREBP-1c, ChREBPα, and the newly identified shorter isoform ChREBPβ. Furthermore, glucose-dependent increases in LXR/retinoid X receptor-regulated luciferase activity driven by the ChREBPα promoter was mediated, at least in part, by O-GlcNAc transferase (OGT) signaling in Huh7 cells. Moreover, we show that LXR and OGT interact and colocalize in the nucleus and that loss of LXRs profoundly reduced nuclear O-GlcNAc signaling and ChREBPα promoter binding activity in vivo. In summary, our study provides evidence that LXRs act as nutrient and glucose metabolic sensors upstream of ChREBP by modulating GK expression, nuclear O-GlcNAc signaling, and ChREBP expression and activity.
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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.