Evidence map›Paper›PMID 26064993›Full record

ArticleJournal of diabetes research2015

Testicular Metabolic Reprogramming in Neonatal Streptozotocin-Induced Type 2 Diabetic Rats Impairs Glycolytic Flux and Promotes Glycogen Synthesis.

L Rato, M G Alves, T R Dias, J E Cavaco, Pedro F Oliveira

Open access · goldAbstract read
In one paragraph

Article in Journal of diabetes research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
9.3field-weighted citation impact, top 2% 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

22 citing papers in PubMed, 70 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

5 authors at 3 institutions in 3 countries.

L RatoHealth Sciences Research Centre (CICS), Faculty of Health Sciences, University of Beira Interior (UBI), Covilhã, Portugal.
M G AlvesHealth Sciences Research Centre (CICS), Faculty of Health Sciences, University of Beira Interior (UBI), Covilhã, Portugal ; Department of Life Sciences, Faculty of Sciences and Technology and Center for Neurosciences and Cell Biology (CNC), University of Coimbra, Portugal.
T R DiasHealth Sciences Research Centre (CICS), Faculty of Health Sciences, University of Beira Interior (UBI), Covilhã, Portugal.
J E CavacoHealth Sciences Research Centre (CICS), Faculty of Health Sciences, University of Beira Interior (UBI), Covilhã, Portugal.
Pedro F OliveiraHealth Sciences Research Centre (CICS), Faculty of Health Sciences, University of Beira Interior (UBI), Covilhã, Portugal ; Department of Microscopy, Laboratory of Cell Biology, Abel Salazar Institute of Biomedical Sciences (ICBAS), University of Porto, Portugal ; Unit for Multidisciplinary Research in Biomedicine (UMIB), Abel Salazar Institute of Biomedical Sciences (ICBAS), University of Porto (UP), Portugal.
University of Beira Interior · PTCenter for Neurosciences · USInstitute of Biomedical Science · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Defects in testicular metabolism are directly implicated with male infertility, but most of the mechanisms associated with type 2 diabetes- (T2DM) induced male infertility remain unknown. We aimed to evaluate the effects of T2DM on testicular glucose metabolism by using a neonatal-streptozotocin- (n-STZ) T2DM animal model. Plasma and testicular hormonal levels were evaluated using specific kits. mRNA and protein expression levels were assessed by real-time PCR and Western Blot, respectively. Testicular metabolic profile was assessed by (1)H-NMR spectroscopy. T2DM rats showed increased glycemic levels, impaired glucose tolerance and hyperinsulinemia. Both testicular and serum testosterone levels were decreased, whereas those of 17β-estradiol were not altered. Testicular glycolytic flux was not favored in testicles of T2DM rats, since, despite the increased expression of both glucose transporters 1 and 3 and the enzyme phosphofructokinase 1, lactate dehydrogenase activity was severely decreased contributing to lower testicular lactate content. However, T2DM enhanced testicular glycogen accumulation, by modulating the availability of the precursors for its synthesis. T2DM also affected the reproductive sperm parameters. Taken together these results indicate that T2DM is able to reprogram testicular metabolism by enhancing alternative metabolic pathways, particularly glycogen synthesis, and such alterations are associated with impaired sperm parameters.

Indexed as

AnimalsDiabetes Mellitus, ExperimentalEstradiolGlucoseGlucose IntoleranceGlucose Transporter Type 1Glucose Transporter Type 3GlycogenGlycolysisL-Lactate DehydrogenaseMaleOxidation-ReductionOxidative StressPhosphofructokinase-1RatsRats, WistarEstradiolGlucoseGlucose Transporter Type 1Glucose Transporter Type 3GlycogenL-Lactate DehydrogenasePhosphofructokinase-1Testosterone

Identifiers

PMID26064993
PMCPMC4443934
OpenAlexW1603272910

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.