ArticleEndocrine2003
Rat strain specific attenuation of estrogen action in the anterior pituitary gland by dietary energy restriction.
Article in Endocrine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 6 citations in OpenAlex.
- Tissue-specific actions of the Ept1, Ept2, Ept6, and Ept9 genetic determinants of responsiveness to estrogens in the female rat.Endocrinology · 2008Article
- Genetic control of estrogen action in the rat: mapping of QTLs that impact pituitary lactotroph hyperplasia in a BN x ACI intercross.Mammalian genome : official journal of the International Mammalian Genome Society · 2007Article
- Genetic mapping of loci controlling diethylstilbestrol-induced thymic atrophy in the Brown Norway rat.Mammalian genome : official journal of the International Mammalian Genome Society · 2006Article
- Article
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 at 2 institutions in 1 country.
Funding
Abstract
The purpose of this study was to compare the effects of a 40% restriction of dietary energy consumption, relative to that consumed by rats allowed to feed ad libitum, on the ability of 17beta-estradiol (E2) to induce pituitary tumorigenesis in two inbred rat strains, ACI and Copenhagen (COP), which are very closely related genetically. Ovary-intact ACI and COP rats were fed either a control or an energy-restricted diet beginning at 8 wk of age. Continuous treatment with E2, released from subcutaneous Silastic tubing implants, was initiated at 9 wk of age and the animals were killed 12 wk later. Estrogen-induced pituitary tumorigenesis is associated with rapid induction of lactotroph hyperplasia, increased pituitary mass, and hyperprolactinemia. E2 significantly increased pituitary mass and circulating prolactin (PRL) in both ACI and COP rats, and this response was significantly greater in ACI rats relative to COP. Dietary energy restriction did not inhibit E2-induced pituitary growth in the ACI rat. By contrast, E2-induced pituitary growth in COP rats was attenuated by dietary energy restriction, as evidenced by quantification of pituitary mass, pituitary weight to body weight ratio, circulating PRL, and pituitary cell proliferation. This study indicates that sensitivity to the inhibitory actions of dietary energy restriction on E2-induced pituitary tumorigenesis is genetically determined.
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What OpenQuestion 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 OpenQuestion graph.