ArticleProceedings of the National Academy of Sciences of the United States of America2026
Hypothalamic endoplasmic reticulum stress drives pubertal precocity due to early-onset obesity in female rodents.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Hypothalamic regulation of energy homeostasis: Quo vadis.Reviews in endocrine & metabolic disorders · 2026Review
- Hypothalamic endoplasmic reticulum stress drives pubertal precocity due to early-onset obesity in female rodents.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
Abstract
Early-onset obesity, especially in girls, is frequently associated with advanced puberty; a phenomenon bound to increased risk of long-term complications. Hypothalamic endoplasmic reticulum (ER) stress has been implicated in the pathophysiology of obesity and its comorbidities. However, its contribution to pubertal disorders associated with obesity remains unexplored. We report herein that central ER stress drives obesity-induced precocious female puberty. Hypothalamic expression of key ER stress markers was blunted during normal pubertal transition and altered in female rats with early-onset obesity and advanced puberty, which displayed increased levels of p-PERK and p-eIF2α, and reduced ATF6α content. Central stimulation of hypothalamic ER stress with Thapsigargin in prepuberal lean female rats mimicked advanced puberty onset caused by obesity, without changes in body weight. This phenomenon seemingly involves a circuit including the hypothalamic arcuate nucleus (ARC), since obesity-induced precocious puberty was largely prevented by alleviation of ER stress via virogenetic overexpression of the ER chaperone, GRP78, in the ARC, but not in the paraventricular nucleus, in female rats. In addition, expression analyses of ER stress markers in mouse Kiss1 neurons isolated from juvenile and pubertal female mice revealed increased expression of
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.