ArticlePloS one2022
Butyrate ameliorates maternal high-fat diet-induced fetal liver cellular apoptosis.
Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Gestational Inulin Supplementation in Low-/High-Fat Sow Diets: Effects on Growth Performance, Lipid Metabolism, and Meat Quality of Offspring Pigs.Foods (Basel, Switzerland) · 2025Article
- Maternal Nutrition, Toxicants, and Epigenetic Programming of Obesity Across Generations.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Review
- Impact of Ionizing Radiation Exposure on Placental Function and Implications for Fetal Programming.International journal of molecular sciences · 2024Review
- Microbiota-derived short chain fatty acids in pediatric health and diseases: from gut development to neuroprotection.Frontiers in microbiology · 2024Review
- The Bacterial DNA Profiling of Chorionic Villi and Amniotic Fluids Reveals Overlaps with Maternal Oral, Vaginal, and Gut Microbiomes.International journal of molecular sciences · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
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Abstract
A maternal high-fat diet (HFD) can impact the offspring's development of liver steatosis, with fetal development in utero being a crucial period. Therefore, this study investigated the mechanism and whether butyrate can rescue liver injury caused by maternal HFD in the fetus. Pregnant female Sprague Dawley rats were randomly divided into two groups, prenatal HFD (58% fat) exposure or normal control diet (4.5% fat). The HFD group was fed an HFD 7 weeks before mating and during gestation until sacrifice at gestation 21 days. After confirmation of mating, the other HFD group was supplemented with sodium butyrate (HFSB). The results showed that maternal liver histology showed lipid accumulation with steatosis and shortened ileum villi in HFD, which was ameliorated in the HFSB group (P<0.05). There was increased fetal liver and ileum TUNEL staining and IL-6 expression with increased fetal liver TNF-α and malondialdehyde expression in the HFD group (P<0.05), which decreased in the HFSB group (P<0.05). The fetal liver expression of phospho-AKT/AKT and GPX1 decreased in the HFD group but increased in the HFSB group (P<0.05). In conclusion that oxidative stress with inflammation and apoptosis plays a vital role after maternal HFD in the fetus liver that can be ameliorated with butyrate supplementation.
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