ArticleThe American journal of pathology2019
N-Acetylcysteine Resolves Placental Inflammatory-Vasculopathic Changes in Mice Consuming a High-Fat Diet.
Article in The American journal of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Delineating the effects of prenatal oxycodone exposure and melatonin treatment on placental and fetal outcomes in pregnant rats.bioRxiv : the preprint server for biology · 2026Article
- Metabolic Reprogramming Driven by Trophoblasts and Decidual XCR1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Maternal high-fat, high-sucrose diet-induced excess adiposity is linked to placental hypoxia and disruption of fetoplacental immune homeostasis in late gestation†.Biology of reproduction · 2025Article
- Maternal Diet-Induced Excess Adiposity in Mice Disrupts Mid-Gestation Decidual Immune and Vascular Homeostasis Without Impairing Spiral Artery Remodeling.Acta physiologica (Oxford, England) · 2025Article
- Potential Effects of Selenium and N-Acetylcysteine Supplementation in Ameliorating Cardinal Symptoms of Nω-Nitro-L-Arginine Methyl Ester Hydrochloride (L-NAME) Induced Preeclampsia in Wistar Rats.Reports of biochemistry & molecular biology · 2025Article
- Article
- Palmitic Acid Impedes Extravillous Trophoblast Activity by Increasing MRP1 Expression and Function.Biomolecules · 2022Article
- Review
- In vivo isotope tracing reveals the versatility of glucose as a brown adipose tissue substrate.Cell reports · 2021Article
- Antioxidant Effects of N-Acetylcysteine Prevent Programmed Metabolic Disease in Mice.Diabetes · 2020Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
The mechanism by which poor maternal nutrition can affect the long-term health of offspring is poorly understood. In mice, we previously found that maternal high-fat diet (HFD) exposure results in reduced fetal growth regardless of maternal genotype. We tested our hypothesis that maternal HFD-induced inflammation contributes to metabolic disease susceptibility of the offspring via alterations in the placenta. The effect of maternal genotype, diet, and treatment with the anti-inflammatory compound N-acetylcysteine (NAC) on placental morphologic features was investigated. Placentas from wild-type dams maintained on a HFD but not those heterozygous (+/-) for Glut4 (Slc2a4) on the same diet had an increase in decidual inflammation and vasculopathy occurring together. NAC administration resulted in amelioration of HFD-induced decidual vasculopathy independent of offspring genotype and sex. Consistent with these morphologic improvements, placentas from HFD dams treated with NAC had decreased mRNA and immunostaining of IL-1β and monocyte chemoattractant protein-1, decreased mRNA of inflammatory genes, and increased mRNA of Vegfa. These results strongly suggest consumption of an HFD results in vascular changes in placenta reflected by alterations in expression of pivotal vascular developmental markers and inflammatory genes all of which are ameliorated by NAC. These placental changes play a key role in the increased programed metabolic disease of HFD-exposed offspring.
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