ArticleHepatology communications2018
Perinatal Nutritional Reprogramming of the Epigenome Promotes Subsequent Development of Nonalcoholic Steatohepatitis.
Article in Hepatology communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 29 citations in OpenAlex.
- Lifespan approaches for the prevention and management of steatotic liver disease.Nature reviews. Gastroenterology & hepatology · 2026Review
- Maternal Dyslipidaemia Aggravates Offspring Metabolic Dysfunction-Associated Steatotic Liver Disease.Basic & clinical pharmacology & toxicology · 2026Article
- Maternal obesogenic diet exposure regulates the offspring gut liver axis and fibroinflammatory liver disease.Communications biology · 2025Article
- MASLD in children: integrating epidemiological trends with mechanistic and translational advances.The Journal of clinical investigation · 2025Review
- Envisioning how to advance the MASH field.Nature reviews. Gastroenterology & hepatology · 2024Review
- Glycogen synthase kinase 3 activity enhances liver inflammation in MASH.JHEP reports : innovation in hepatology · 2024Article
- Maternal Obesogenic Diet Attenuates Microbiome-Dependent Offspring Weaning Reaction with Worsening of Steatotic Liver Disease.The American journal of pathology · 2024Article
- Article
- Maternal Weight Management to Prevent the Developmental Programming of MAFLD in Offspring of Obese Mothers.Nutrients · 2023Review
- Prenatal Choline Supplement in a Maternal Obesity Model Modulates Offspring Hepatic Lipidomes.Nutrients · 2023Article
- Maternal Exercise Protects Male Offspring From Maternal Diet-Programmed Nonalcoholic Fatty Liver Disease Progression.Endocrinology · 2023Article
- Maternal obesogenic diet regulates offspring bile acid homeostasis and hepatic lipid metabolism via the gut microbiome in mice.American journal of physiology. Gastrointestinal and liver physiology · 2022Article
- The Origins of NAFLD: The Potential Implication of Intrauterine Life and Early Postnatal Period.Cells · 2022Review
- Liver sinusoidal endothelial cell expressed vascular cell adhesion molecule 1 promotes liver fibrosis.Frontiers in immunology · 2022Article
- Review
- Hepatic Steatosis in Infancy: The Beginning of Pediatric Nonalcoholic Fatty Liver Disease?JPGN reports · 2021Article
- Perspectives on youth-onset nonalcoholic fatty liver disease.Endocrinology, diabetes & metabolism · 2020Review
- Developmental Programming of NAFLD by Parental Obesity.Hepatology communications · 2020Review
- Review
- Fructose-mediated effects on gene expression and epigenetic mechanisms associated with NAFLD pathogenesis.Cellular and molecular life sciences : CMLS · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
With the epidemic of obesity, nonalcoholic fatty liver disease (NAFLD) has become the most common pediatric liver disease. The influence of a perinatal obesity-inducing diet (OID) on the development and progression of NAFLD in offspring is important but incompletely studied. Hence, we fed breeding pairs of C57BL/6J mice during gestation and lactation (perinatally) either chow or an OID rich in fat, fructose, and cholesterol (FFC). The offspring were weaned to either chow or an FFC diet, generating four groups: perinatal (p)Chow-Chow, pChow-FFC, pFFC-Chow, and pFFC-FFC. Mice were sacrificed at 10 weeks of age. We examined the whole-liver transcriptome by RNA sequencing (RNA-seq) and whole-liver genome methylation by reduced representation bisulfite sequencing (RRBS). Our results indicated that the pFFC-FFC mice had a significant increase in hepatic steatosis, injury, inflammation, and fibrosis, as assessed histologically and biochemically. We identified 189 genes that were differentially expressed and methylated in the pFFC-FFC mice versus the pChow-FFC mice. Gene set enrichment analysis identified hepatic fibrosis/hepatic stellate cell activation as the top canonical pathway, suggesting that the differential DNA methylation events in the mice exposed to the FFC diet perinatally were associated with a profibrogenic transcriptome. To verify that this finding was consistent with perinatal nutritional reprogramming of the methylome, we exposed pFFC-Chow mice to an FFC diet in adulthood. These mice developed significant hepatic steatosis, injury, inflammation, and more importantly fibrosis when compared to the appropriate controls.
Identifiers
What OpenQuestion holds
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.