ArticlePediatric research2019
Dlk1 expression relates to visceral fat expansion and insulin resistance in male and female rats with postnatal catch-up growth.
Article in Pediatric research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Association of DLK1-MEG3 methylation levels in cord blood with small for gestational age.Pediatric research · 2026Article
- Silencing YTHDF2 Induces Apoptosis of Neuroblastoma Cells In a Cell Line-Dependent Manner via Regulating the Expression of DLK1.Molecular neurobiology · 2025Article
- The Fetal Environment and the Development of Hypertension-The Epigenetic Modification by Glucocorticoids.International journal of molecular sciences · 2025Review
- scParser: sparse representation learning for scalable single-cell RNA sequencing data analysis.Genome biology · 2024Article
- Article
- Gestational Caloric Restriction Alters Adipose Tissue Methylome and Offspring's Metabolic Profile in a Swine Model.International journal of molecular sciences · 2024Article
- Biomarkers for Diagnosing and Treating Fetal Growth Restriction.Current medicinal chemistry · 2024Review
- Familial central precocious puberty due to DLK1 deficiency: novel genetic findings and relevance of serum DLK1 levels.European journal of endocrinology · 2023Article
- Catch-up growth in juvenile rats, fat expansion, and dysregulation of visceral adipose tissue.Pediatric research · 2022Article
- Circulating levels of DLK1 and glucose homeostasis in girls with obesity: A pilot study.Frontiers in endocrinology · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlthough prenatal and postnatal programming of metabolic diseases in adulthood is well established, the mechanisms underpinning metabolic programming are not. Dlk1, a key regulator of fetal development, inhibits adipocyte differentiation and restricts fetal growth.
methodsAssess DLk1 expression in a Wistar rat model of catch-up growth following intrauterine restriction. Dams fed ad libitum delivered control pups (C) and dams on a 50% calorie-restricted diet delivered pups with low birth weight (R). Restricted offspring fed a standard rat chow showed catch-up growth (R/C) but those kept on a calorie-restricted diet did not (R/R).
resultsDecreased Dlk1 expression was observed in adipose tissue and skeletal muscle of R/C pups along with excessive visceral fat accumulation, decreased circulating adiponectin, increased triglycerides and HOMA-IR (from p < 0.05 to p < 0.0001). Moreover, in R/C pups the reduced Dlk1 expression in adipose tissue and skeletal muscle correlated with visceral fat (r = -0.820, p < 00001) and HOMA-IR (r = -0.745, p = 0.002).
conclusionsDecreased Dlk1 expression relates to visceral fat expansion and insulin resistance in a rat model of catch-up growth following prenatal growth restriction. Modulation of Dlk1 expression could be among the targets for the early prevention of fetal programming of adult metabolic disorders.
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