Loading
Life sciences · Journal article
Archives of Medical Research · October 26, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Background Abnormal intestinal morphology and dysbiosis contribute to metabolic disease development. Maternal obesity increases offspring susceptibility to gut dysfunction. The α7 nicotinic acetylcholine receptor (α7nAChR), encoded by Chrna7, is a key mediator of the cholinergic anti-inflammatory pathway and modulates intestinal immunity and cell proliferation. However, the role of cholinergic signaling in offspring intestinal development remains unclear. Methods 5-week-old female C57BL/6 mice were fed a control (SC, 10% fat) or a high-fat diet (HFD, 45% fat) before and during pregnancy and lactation. The small intestines of fetal (e20) offspring were analyzed for inflammatory markers and tight junctions (Claudin-1, Claudin-2, Occludin, Zonula occludens-1). Additional evaluations at weaning (d28) included histomorphometry, intestinal transit and permeability assays, and microbiota analysis. Chrna7⁻ / ⁻ mice were evaluated for histomorphometry and intestinal permeability. Results Maternal HFD disrupted the intestinal morphology and function of offspring, resulting in shorter villi, reduced mucosal thickness and goblet cell proportion, reduced α7nAChR expression, and increased permeability. While male HFD-O exhibited an increased Firmicutes/Bacteroidetes ratio, female HFD-O presented a significant reduction in Akkermansia and Verrucomicrobiota abundance, though they displayed an early adaptive response in tight junction expression at e20. Chrna7 ⁻ / ⁻ mice exhibited similar intestinal morphological alterations, recapitulating most features observed in offspring of HFD-fed dams. Conclusions Maternal HFD programs a vulnerable intestinal phenotype in offspring characterized by significant structural and moderate functional and microbiota reprogramming. The phenotypic similarities between HFD-O and Chrna7 –/– suggest a potential involvement of this receptor in shaping offspring gut health, offering potential targets to prevent diet-induced intestinal dysfunctions.