Evidence map›Paper›PMID 32375121›Full record

ArticleEndocrine connections2020

Sam68 mediates leptin signaling and action in human granulosa cells: possible role in leptin resistance in PCOS.

Teresa Vilariño-García, Antonio Pérez-Pérez, Esther Santamaría-López, Nicolás Prados, Manuel Fernández-Sánchez, Víctor Sánchez-Margalet

Open access · goldAbstract read
In one paragraph

Article in Endocrine connections, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Role of Sam68 in different types of cancer (Review).International journal of molecular medicine · 2025
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  13. Insulin resistance and PCOS: chicken or egg?Journal of endocrinological investigation · 2021
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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

6 authors at 2 institutions in 1 country.

Teresa Vilariño-GarcíaDepartment of Medical Biochemistry, Molecular Biology and Immunology. Medical School, Virgen Macarena University Hospital, University of Seville, Seville, Spain.
Antonio Pérez-PérezDepartment of Medical Biochemistry, Molecular Biology and Immunology. Medical School, Virgen Macarena University Hospital, University of Seville, Seville, Spain.
Esther Santamaría-LópezValencian Infertility Institute (IVI), Seville, Spain.
Nicolás PradosValencian Infertility Institute (IVI), Seville, Spain.
Manuel Fernández-SánchezValencian Infertility Institute (IVI), Seville, Spain.
Víctor Sánchez-MargaletDepartment of Medical Biochemistry, Molecular Biology and Immunology. Medical School, Virgen Macarena University Hospital, University of Seville, Seville, Spain.
Universidad de Sevilla · ESValencian Infertility Institute · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionPolycystic ovary syndrome (PCOS) is a complex metabolic disorder associated with ovulatory dysfunction, hyperandrogenism, obesity, and insulin resistance, that leads to subfertility. Sam68 is an RNA-binding protein with signaling functions that is ubiquitously expressed, including gonads. Sam68 is recruited to leptin signaling, mediating different leptin actions.

objectiveWe aimed to investigate the role of Sam68 in leptin signaling, mediating the effect on aromatase expression in granulosa cells and the posible implication of Sam68 in the leptin resistance in PCOS. MATERIALS AND

methodsGranulosa cells were from healthy donors (n = 25) and women with PCOS (n = 25), within the age range of 20 to 40 years, from Valencian Infertility Institute (IVI), Seville, Spain. Sam68 expression was inhibited by siRNA method and overexpressed by expression vector. Expression level was analysed by qPCR and immunoblot. Statistical significance was assessed by ANOVA followed by different post-hoc tests. A P value of <0.05 was considered statistically significant.

resultsWe have found that leptin stimulation increases phosphorylation and expression level of Sam68 and aromatase in granulosa cells from normal donors. Downregulation of Sam68 expression resulted in a lower activation of MAPK and PI3K pathways in response to leptin, whereas overexpression of Sam68 increased leptin stimulation of signaling, enhancing aromatase expression. Granulosa cells from women with PCOS presented lower expression of Sam68 and were resistant to the leptin effect on aromatase expression.

conclusionsThese results suggest the participation of Sam68 in leptin receptor signaling, mediating the leptin effect on aromatase expression in granulosa cells, and point to a new target in leptin resistance in PCOS.

Indexed as

aromataseleptinpolycystic ovary syndrome (PCOS)Sam68signalling pathways

Identifiers

PMID32375121
PMCPMC7354740
OpenAlexW3021206299

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.