Evidence map›Paper›PMID 26122485›Full record

ArticleJournal of endocrinological investigation2016

D-Aspartic acid stimulates steroidogenesis through the delay of LH receptor internalization in a mammalian Leydig cell line.

A Di Nisio, L De Toni, M Ferigo, M S Rocca, E Speltra, A Ferlin, C Foresta

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Journal of endocrinological investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

A Di NisioDepartment of Medicine, Section of Endocrinology and Centre for Human Reproduction Pathology, University of Padova, Via Giustiniani, 2, 35128, Padua, Italy.
L De ToniDepartment of Medicine, Section of Endocrinology and Centre for Human Reproduction Pathology, University of Padova, Via Giustiniani, 2, 35128, Padua, Italy.
M FerigoDepartment of Molecular Medicine, University of Padova, Padua, Italy.
M S RoccaDepartment of Medicine, Section of Endocrinology and Centre for Human Reproduction Pathology, University of Padova, Via Giustiniani, 2, 35128, Padua, Italy.
E SpeltraDepartment of Medicine, Section of Endocrinology and Centre for Human Reproduction Pathology, University of Padova, Via Giustiniani, 2, 35128, Padua, Italy.
A FerlinDepartment of Medicine, Section of Endocrinology and Centre for Human Reproduction Pathology, University of Padova, Via Giustiniani, 2, 35128, Padua, Italy.
C ForestaDepartment of Medicine, Section of Endocrinology and Centre for Human Reproduction Pathology, University of Padova, Via Giustiniani, 2, 35128, Padua, Italy. carlo.foresta@unipd.it.
University of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeRecent experimental evidence on non-mammalian animal models showed that D-Aspartic acid (d-Asp) administration increases testosterone levels through upregulation of StAR in Leydig cells. In this study, we aimed to investigate in vitro the signaling pathway associated with d-Asp stimulation in MA-10 murine Leydig cells.

methodsMA-10 cells were stimulated with different concentrations of d-Asp, in presence or absence of hCG. Then total testosterone (T) levels in the culture medium were evaluated by electrochemiluminescence immunoassay, and StAR and LHR protein expressions were quantified by the means of Western blotting. LHR cellular localization after hormonal stimulation was assessed by immunofluorescence.

resultsStimulation with the sole d-Asp did not induce any relevant increase of T release from cultured cells. On the other hand, stimulation with hCG induced significant increase of T (P = 0.045). Concomitant stimulation with hCG and d-Asp, at the concentration of 0.1 and 1 nM, induced additional and significant increase of released T (P = 0.03 and P = 0.04, respectively). StAR protein levels increased after concomitant stimulation with hCG and d-Asp 0.1 nM, compared with stimulation with the sole hCG (P = 0.02), whereas no variation in LHR protein expression was observed. Finally, d-Asp attenuated displacement of LHR staining, from cell membrane to cytoplasm, subsequent to hCG stimulation.

conclusionsIn this study, we confirmed a steroidogenic role for d-Asp, in concert with hCG, on murine Leydig cells, which is mediated by an increase in StAR protein levels. In addition, we showed that the possible mechanism subtending the effect of d-Asp could rely on the modulation of LHR exposure on the cell membrane.

Indexed as

AnimalsCell LineCell MembraneChorionic GonadotropinClone CellsD-Aspartic AcidHumansKineticsLeydig CellsMaleMembrane Transport ModulatorsMiceMicroscopy, FluorescenceMicroscopy, VideoPhosphoproteinsProtein TransportChorionic GonadotropinD-Aspartic AcidMembrane Transport ModulatorsPhosphoproteinsReceptors, LHReproductive Control AgentsSteroidogenic Acute Regulatory ProteinTestosteroneD-Aspartic acidLeydig cellsLH receptor internalizationSteroidogenesisTestosterone

Identifiers

PMID26122485
OpenAlexW802387885

What OpenQuestion holds

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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.