ArticleComputational and mathematical methods in medicine2022
PRL/PRLR Can Promote Insulin Resistance by Activating the JAK2/STAT5 Signaling Pathway.
Article in Computational and mathematical methods in medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 3 papers.
What it found
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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
3 citing papers in PubMed, 6 citations in OpenAlex.
- Dopamine receptor agonists mechanism of actions on glucose lowering and their connections with prolactin actions.Frontiers in clinical diabetes and healthcare · 2023Review
- Retracted: PRL/PRLR Can Promote Insulin Resistance by Activating the JAK2/STAT5 Signaling Pathway.Computational and mathematical methods in medicine · 2023Article
- Preliminary evaluation of the antiglycoxidant activity of verapamil using variousFrontiers in pharmacology · 2023Article
Corrections and comments
- Retraction · 2023-11-29Compromised Peer Review · Investigation by Journal/Publisher · Investigation by Third Party · Paper Mill · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Although prolactin (PRL) is known to affect food intake, weight gain, and insulin resistance, its effects on lipid metabolism and underlying mechanisms remain underinvestigated. This study aimed to investigate the effects of PRL and its receptor (PRLR) on fat metabolism in regulating the JAK2/STAT5 signaling pathway. Methods: SW872 adipocytes were incubated with oleic acid to establish an insulin resistance (IR) model. Western blot was used to detect the expression of PRLR, JAK2, p-JAK2, STAT5, and p-STAT5. Triglyceride (TG) mass was detected by chemical colorimetry methods. Results: Fat droplets in the high-dose and medium-dose PRL groups were significantly higher than in the IR model group. TG mass in the cells was increased significantly compared with the model group. Compared with the control group, the expression of PRLR, p-JAK2, and p-STAT5 were significantly decreased in the IR model group when PRL was intervened for 24 h and 48 h. The expression of PRLR, p-JAK2, and p-STAT5 in the high-dose PRL intervention group increased significantly compared with the model group. The PRLR overexpressing group had significantly increased TG content and PRLR, and JAK2, p-JAK2, STAT5, and p-STAT5 levels compared with the IR model. Conclusion: PRL and PRLR are related to fat metabolism, and the PRL/PRLR signaling pathway can promote insulin resistance by activating the JAK2/STAT5 signaling pathway and increasing the deposition of TGs.
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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.