ArticleThe Journal of physiology2026
Maternal obesity during pregnancy disrupts iron homeostasis and promotes fetal hypoxia in the mouse.
Article in The Journal of physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Research in both humans and animals has consistently demonstrated that diverse complications during pregnancy impact on the risk of chronic diseases in the offspring. In many settings, over half of women are either overweight or living with obesity during pregnancy. This has short- and long-term impacts on offspring health. The mechanisms mediating changes in the fetal environment that may trigger developmental origins of future cardiometabolic risk in the offspring are not fully elucidated. In this study, using an established mouse model, we aimed to determine whether obesity during pregnancy causes fetal hypoxia and to explore potential underlying mechanisms. We showed that fetal hypoxia is a key component of the in utero obesogenic environment at E13.5/0.7 of gestation. Concomitantly, obese dams exhibit low iron levels, as well as higher circulating levels of hepcidin and C-reactive protein. We also showed that placental structure and efficiency are not affected by maternal obesity at E13.5, suggesting that the reduction in oxygen delivery to the fetus was not a consequence of placental dysfunction at this stage of gestation. We conclude that maternal obesity-induced iron deficiency and fetal hypoxia are important mechanisms by which obesity during pregnancy impacts offspring health. Furthermore, iron deficiency in mothers with obesity is a tractable therapeutic target for intervention that could prevent transmission of poor cardiometabolic health from mother to child. KEY POINTS: Diet-induced maternal obesity resulted in fetal, but not placental, hypoxia. Pregnant mice with obesity had lower circulating iron levels, along with dysregulation of key molecules involved in iron homeostasis, such as transferrin and the hormone hepcidin. Body weight, fat mass, circulating insulin and hepcidin levels in mothers with obesity were significantly correlated with the degree of fetal hypoxia, suggesting they were interrelated.
Indexed as
Identifiers
What Socratic 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 Socratic graph.