ArticleScientific reports2016
Foetal programming by methyl donor deficiency produces steato-hepatitis in rats exposed to high fat diet.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 20 citations in OpenAlex.
- Effects of Maternal Nutrition and One-Carbon Metabolite Supplementation on Fetal Jejunal Morphology and Hexose Transporter Expression in Beef Cattle.Veterinary sciences · 2025Article
- Long term links between maternal diet during pregnancy and offspring health.Pediatric research · 2025Review
- Folic Acid and Methyltetrahydrofolate Supplementation in theNutrients · 2024Article
- Pregnancy homocysteine and cobalamin status predict childhood metabolic health in the offspring.Pediatric research · 2023Article
- Maternal dietary methionine restriction alters hepatic expression of one-carbon metabolism and epigenetic mechanism genes in the ducklings.BMC genomics · 2022Article
- Sirt1-PPARS Cross-Talk in Complex Metabolic Diseases and Inherited Disorders of the One Carbon Metabolism.Cells · 2020Review
- Preconception paternal alcohol exposure exerts sex-specific effects on offspring growth and long-term metabolic programming.Epigenetics & chromatin · 2019Article
- DNA methylation-independent growth restriction and altered developmental programming in a mouse model of preconception male alcohol exposure.Epigenetics · 2017Article
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Authors and funding
15 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Non-alcoholic steatohepatitis (NASH) is a manifestation of metabolic syndrome, which emerges as a major public health problem. Deficiency in methyl donors (folate and vitamin B12) during gestation and lactation is frequent in humans and produces foetal programming effects of metabolic syndrome, with small birth weight and liver steatosis at day 21 (d21), in rat pups. We investigated the effects of fetal programming on liver of rats born from deficient mothers (iMDD) and subsequently subjected to normal diet after d21 and high fat diet (HF) after d50. We observed increased abdominal fat, ASAT/ALAT ratio and angiotensin blood level, but no histological liver abnormality in d50 iMDD rats. In contrast, d185 iMDD/HF animals had hallmarks of steato-hepatitis, with increased markers of inflammation and fibrosis (caspase1, cleaved IL-1β, α1(I) and α2(I) collagens and α-SMA), insulin resistance (HOMA-IR and Glut 2) and expression of genes involved in stellate cell stimulation and remodelling and key genes triggering NASH pathomechanisms (transforming growth factor beta super family, angiotensin and angiotensin receptor type 1). Our data showed a foetal programming effect of MDD on liver inflammation and fibrosis, which suggests investigating whether MDD during pregnancy is a risk factor of NASH in populations subsequently exposed to HF diet.
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