Evidence map›Paper›PMID 33746901›Full record

ArticleFrontiers in endocrinology2021

Global Deletion of the Prolactin Receptor Aggravates Streptozotocin-Induced Diabetes in Mice.

Gabriela Ramirez-Hernandez, Elva Adan-Castro, Nundehui Diaz-Lezama, Xarubet Ruiz-Herrera, Gonzalo Martinez de la Escalera, Yazmin Macotela, Carmen Clapp

Open access · goldAbstract read
In one paragraph

Article in Frontiers in endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

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  12. The beneficial metabolic actions of prolactin.Frontiers in endocrinology · 2022
    Review
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

7 authors at 1 institution in 1 country.

Gabriela Ramirez-HernandezInstituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Querétaro, Mexico.
Elva Adan-CastroInstituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Querétaro, Mexico.
Nundehui Diaz-LezamaInstituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Querétaro, Mexico.
Xarubet Ruiz-HerreraInstituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Querétaro, Mexico.
Gonzalo Martinez de la EscaleraInstituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Querétaro, Mexico.
Yazmin MacotelaInstituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Querétaro, Mexico.
Carmen ClappInstituto de Neurobiología, Universidad Nacional Autónoma de México (UNAM), Querétaro, Mexico.
Universidad Nacional Autónoma de México · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prolactin (PRL) levels are reduced in the circulation of rats with diabetes or obesity, and lower circulating levels of PRL correlate with increased prevalence of diabetes and a higher risk of metabolic alterations in the clinic. Furthermore, PRL stimulates β-cell proliferation, survival, and insulin production and pregnant mice lacking PRL receptors in β-cells develop gestational diabetes. To investigate the protective effect of endogenous PRL against diabetes outside pregnancy, we compared the number of cases and severity of streptozotocin (STZ)-induced hyperglycemia between C57BL/6 mice null for the PRL receptor gene (

Indexed as

AnimalsBlood GlucoseCell ProliferationCell SurvivalDiabetes Mellitus, ExperimentalGlucose IntoleranceInsulinInsulin-Secreting CellsMiceReceptors, ProlactinBlood GlucoseInsulinReceptors, Prolactinbeta-cellglucose homeostasisprolactinprolactin receptor null miceSTZ-induced diabetes

Identifiers

PMID33746901
PMCPMC7973366
OpenAlexW3133706578

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.