ArticleHuman molecular genetics2016
Early hypermethylation of hepatic Igfbp2 results in its reduced expression preceding fatty liver in mice.
Article in Human molecular genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 50 citations in OpenAlex.
- Epigenetic Regulation of PLIN 1 in Obese Women and its Relation to Lipolysis.Scientific reports · 2017Trial
- Serpina3c protects against metabolic dysfunction-associated steatotic liver disease in offspring induced by prenatal prednisone exposure.Signal transduction and targeted therapy · 2026Article
- Insulin-like growth factor binding proteins in metabolic dysfunction-associated steatotic liver disease.Frontiers in endocrinology · 2026Review
- Tissue-specific roles of IGFBP2 in glucose and lipid metabolism in obesity-related metabolic diseases.Frontiers in nutrition · 2026Review
- DNA methylation reshapes the expression of adipokines and adipose factors in white adipose tissues.Epigenetics & chromatin · 2025Review
- Review of roles of RNA-binding proteins on NAFLD and the related pharmaceutical measures.Biomolecules & biomedicine · 2025Review
- Insulin-Like Growth Factors, Binding Proteins and Their Role in Pregnancy in Patients With Diabetes.Journal of diabetes research · 2025Review
- High-temperature exposure during the early embryonic stage lowers core body temperature after growth via a hypothalamic Igfbp2-dependent mechanism.Scientific reports · 2024Article
- IGFBP2 functions as an endogenous protector against hepatic steatosis via suppression of the EGFR-STAT3 pathway.Molecular metabolism · 2024Article
- Medaka liver developed Human NAFLD-NASH transcriptional signatures in response to ancestral bisphenol A exposure.Research square · 2024Article
- Sex-specific expression of the human NAFLD-NASH transcriptional signatures in the liver of medaka with a history of ancestral bisphenol A exposure.bioRxiv : the preprint server for biology · 2024Article
- Tissue explants as tools for studying the epigenetic modulation of the GH-IGF-I axis in farmed fish.Frontiers in physiology · 2024Article
- Goose Hepatic IGFBP2 Is Regulated by Nutritional Status and Participates in Energy Metabolism Mainly through the Cytokine-Cytokine Receptor Pathway.Animals : an open access journal from MDPI · 2023Article
- FGF1 ameliorates obesity-associated hepatic steatosis by reversing IGFBP2 hypermethylation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Loss of IGFBP2 mediates alveolar type 2 cell senescence and promotes lung fibrosis.Cell reports. Medicine · 2023Article
- Diclofenac Disrupts the Circadian Clock and through Complex Cross-Talks Aggravates Immune-Mediated Liver Injury-A Repeated Dose Study in Minipigs for 28 Days.International journal of molecular sciences · 2023Article
- Plasma IGFBP-2 levels reveal heterogeneity in hepatic fat content in adults with excess visceral adiposity.Frontiers in endocrinology · 2023Article
- Transcriptome changes in stages of non-alcoholic fatty liver disease.World journal of hepatology · 2022Article
- Genetic and epigenetic factors determining NAFLD risk.Molecular metabolism · 2021Review
- Non-Alcoholic Fatty Liver Disease: Metabolic, Genetic, Epigenetic and Environmental Risk Factors.International journal of environmental research and public health · 2021Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obesity and ectopic fat disposition are risk factors for metabolic disease. Recent data indicate that IGFBP2 expression in liver is epigenetically inhibited during hepatic steatosis. The aim of this study was to investigate if epigenetic de-regulation of hepatic Igfbp2 occurs already early in life and is associated with increased risk for diet-induced obesity (DIO) during adolescence. Male C57BL/6J mice received a high-fat diet. After 3 weeks on this diet (age of 6 weeks), DIO-susceptible (responder, Resp) and DIO-resistant (non-responder, nResp) mice were identified by early weight gain. At the age of 6 weeks, Resp mice exhibited elevated blood glucose (p < 0.05), plasma insulin (p < 0.01), HOMA-IR and leptin/adiponectin ratio, whereas liver triglycerides were identical but significantly increased (p < 0.01) in Resp mice at 20 weeks of age. Igfbp2 expression was reduced in young Resp compared with nResp mice (p < 0.01), an effect that correlated with elevated DNA methylation of intronic CpG
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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.