Evidence map›Paper›PMID 31697938›Full record

ArticleDevelopmental biology2020

Epithelial-adipocyte interactions are required for mammary gland development, but not for milk production or fertility.

Audrey Brenot, Irina Hutson, Charles Harris

Open access · greenAbstract read
In one paragraph

Article in Developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 16% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 26 citations in OpenAlex.

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  15. Mammary gland adipocytes in lactation cycle, obesity and breast cancer.Reviews in endocrine & metabolic disorders · 2021
    Review
  16. Adipose tissue is a critical regulator of osteoarthritis.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  17. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Audrey BrenotDepartment of Medicine, Divisions of Hematology and Oncology, 660 South Euclid Avenue, Washington University School of Medicine, St. Louis, MO, 63110, United States.
Irina HutsonDepartment of Medicine, Divisions of Endocrinology, Metabolism and Lipid Research, 660 South Euclid Avenue, Washington University School of Medicine, St. Louis, MO, 63110, United States.
Charles HarrisDepartment of Medicine, Divisions of Endocrinology, Metabolism and Lipid Research, 660 South Euclid Avenue, Washington University School of Medicine, St. Louis, MO, 63110, United States; Medicine Service, Division of Endocrinology, St. Louis VA Medical Center, 915 N Grand Avenue, St. Louis, MO, 63106, United States. Electronic address: harrisc@wustl.edu.
Washington University in St. Louis · US

Funding

GLUCOCORTICOID RECEPTOR POST-TRANSLATIONAL MODIFICATIONS IN INSULIN RESISTANCER01DK106083 · NIDDK · WASHINGTON UNIVERSITY · PI SEMENKOVICH, CLAY F. · 2016 to 2020
$1.7M
NIDDK NIH HHS R01 DK106083
6 · The paper itself

Abstract

To investigate the role of adipose tissue in reproductive function and mammary gland development and function, we have examined lipodystrophic (LD) mice. LD mice of both sexes are sterile, but fertility can be restored with leptin injections. Mammary glands from lipodystrophic mice were rudimentary and lacked terminal end buds. Leptin-injected LD mice were able to become pregnant, showed normal pregnancy-associated glandular proliferation despite a smaller glandular area, were able to produce a small amount of milk that had grossly normal content of milk proteins and neutral lipids, but could not sustain pups to weaning. In order to separate the individual requirements for 1) adipokines such as leptin, 2) estradiol, and 3) physical epithelial-adipocyte interactions, we performed a series of experiments with both lipodystrophic mice and ob (obese mice with a mutation in the lep gene encoding the adipokine leptin) mice that received either estradiol treatment or preadipocyte transplant. The resulting fat pad did not rescue the defect in mammary gland development in lipodystrophic mice. The defect also could not be rescued with estradiol pellets. Ob/ob mice, like LD mice, lack leptin and estradiol, but retain adipose tissue. Ob mice have defective mammary gland development. However, in striking contrast to what was observed in lipodystrophic mice, reconstitution of a WT fat pad in ob mice rescued the defect in mammary gland development. Estradiol treatment did not rescue mammary gland development in ob mice. Therefore direct interaction between mammary gland epithelia and adipocytes is a requirement for full invasion and expansion of the gland, but is not required for glandular proliferation during pregnancy and milk production.

Indexed as

AdipocytesAdipose TissueAnimalsEpithelial CellsEstradiolFemaleFertilityLactationLeptinLipodystrophyMammary Glands, AnimalMiceMice, Inbred C57BLMouse Embryonic Stem CellsObesitySignal TransductionEstradiolLeptin

Identifiers

PMID31697938
PMCPMC6995771
OpenAlexW2983115767

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.