Evidence map›Paper›PMID 23775766›Full record

ArticleDiabetes2013

PRLR regulates hepatic insulin sensitivity in mice via STAT5.

Junjie Yu, Fei Xiao, Qian Zhang, Bin Liu, Yajie Guo, Ziquan Lv, Tingting Xia, Shanghai Chen, Kai Li, Ying Du and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

34 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Diagnosis of hypoprolactinemia.Reviews in endocrine & metabolic disorders · 2024
    Review
  7. The molecular basis of hypoprolactinaemia.Reviews in endocrine & metabolic disorders · 2024
    Review
  8. The prolactin receptor (Genes & diseases · 2024
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. The beneficial metabolic actions of prolactin.Frontiers in endocrinology · 2022
    Review
  17. Article
  18. Review
  19. Review
  20. 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

11 authors at 1 institution in 1 country.

Junjie YuKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences, the Graduate School of the Chinese Academy of Sciences, Shanghai, People's Republic of China.
Fei Xiao
Qian Zhang
Bin Liu
Yajie Guo
Ziquan Lv
Tingting Xia
Shanghai Chen
Kai Li
Ying Du
Feifan Guo
Chinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin resistance is one of the major contributing factors in the development of metabolic diseases. The mechanisms responsible for insulin resistance, however, remain poorly understood. Although numerous functions of the prolactin receptor (PRLR) have been identified, a direct effect on insulin sensitivity has not been previously described. The aim of our current study is to investigate this possibility and elucidate underlying mechanisms. Here we show that insulin sensitivity is improved or impaired in mice injected with adenovirus that overexpress or knock down PRLR expression, respectively. Similar observations were obtained in in vitro studies. In addition, we discovered that the signal transducer and activator of transcription-5 pathway are required for regulating insulin sensitivity by PRLR. Moreover, we observed that PRLR expression is decreased or increased under insulin-resistant (db/db mice) or insulin-sensitive (leucine deprivation) conditions, respectively, and found that altering PRLR expression significantly reverses insulin sensitivity under both conditions. Finally, we found that PRLR expression levels are increased under leucine deprivation via a general control nonderepressible 2/mammalian target of rapamycin/ribosomal protein S6 kinase-1-dependent pathway. These results demonstrate a novel function for hepatic PRLR in the regulation of insulin sensitivity and provide important insights concerning the nutritional regulation of PRLR expression.

Indexed as

AnimalsBlotting, WesternCells, CulturedHepatocytesInsulin ResistanceLiverMaleMiceMice, Inbred C57BLMice, KnockoutProtein Serine-Threonine KinasesReceptors, ProlactinReverse Transcriptase Polymerase Chain ReactionRibosomal Protein S6 Kinases, 70-kDaSTAT5 Transcription FactorEif2ak4 protein, mouseProtein Serine-Threonine KinasesReceptors, ProlactinRibosomal Protein S6 Kinases, 70-kDaSTAT5 Transcription Factor

Identifiers

PMID23775766
PMCPMC3749345
OpenAlexW2125725426

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.