Evidence map›Paper›PMID 29971762›Full record

ArticleBritish journal of pharmacology2018

Selegiline reduces adiposity induced by high-fat, high-sucrose diet in male rats.

Csilla Terézia Nagy, Gábor Koncsos, Zoltán V Varga, Tamás Baranyai, Sebestyén Tuza, Ferenc Kassai, Aliz Judit Ernyey, István Gyertyán, Kornél Király, Attila Oláh and 14 more

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

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  10. Selegiline: a molecule with innovative potential.Journal of neural transmission (Vienna, Austria : 1996) · 2020
    Review
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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

24 authors at 4 institutions in 3 countries.

Csilla Terézia NagyDepartment of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Gábor KoncsosDepartment of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Zoltán V VargaDepartment of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Tamás BaranyaiDepartment of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Sebestyén TuzaDepartment of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Ferenc KassaiMTA-SE NAP B Cognitive Translational Behavioural Pharmacology Group, Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Aliz Judit ErnyeyMTA-SE NAP B Cognitive Translational Behavioural Pharmacology Group, Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
István GyertyánMTA-SE NAP B Cognitive Translational Behavioural Pharmacology Group, Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Kornél KirályDepartment of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Attila OláhHeart and Vascular Center, Semmelweis University, Budapest, Hungary.
Tamás RadovitsHeart and Vascular Center, Semmelweis University, Budapest, Hungary.
Béla MerkelyHeart and Vascular Center, Semmelweis University, Budapest, Hungary.
Nóra BukoszaInstitute of Pathophysiology, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Gábor SzénásiInstitute of Pathophysiology, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Péter HamarInstitute of Pathophysiology, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Domokos MathéDepartment of Biophysics and Radiation Biology, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Krisztián SzigetiDepartment of Biophysics and Radiation Biology, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Csilla PelyheDepartment of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Marek JelemenskýInstitute for Heart Research, Centre of Experimental Medicine, Slovak Academy of Sciences, Bratislava, Slovakia.
Zsófia OnódiDepartment of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Zsuzsanna HelyesDepartment of Pharmacology and Pharmacotherapy, Medical School and Szentágothai Research Centre, University of Pécs, Pécs, Hungary.
Rainer SchulzInstitute of Physiology, Justus-Liebig University Giessen, Germany.
Zoltán GiriczDepartment of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary.ORCID 0000-0003-2036-8665
Péter FerdinandyDepartment of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Budapest, Hungary.
Semmelweis University · HUJustus-Liebig-Universität Gießen · DESlovak Academy of Sciences · SKUniversity of Pecs · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeIncidence and severity of obesity are increasing worldwide, however, efficient and safe pharmacological treatments are not yet available. Certain MAO inhibitors reduce body weight, although their effects on metabolic parameters have not been investigated. Here, we have assessed effects of a widely used, selective MAO-B inhibitor, selegiline, on metabolic parameters in a rat model of diet-induced obesity. EXPERIMENTAL APPROACH: Male Long-Evans rats were given control (CON) or a high-fat (20%), high-sucrose (15%) diet (HFS) for 25 weeks. From week 16, animals were injected s.c. with 0.25 mg·kg KEY

resultsSelegiline decreased whole body fat, subcutaneous- and visceral adiposity, measured by CT and epididymal fat weight in the HFS group, compared with HFS placebo animals, without influencing body weight. Oral glucose tolerance and insulin tolerance tests showed impaired glucose homeostasis in HFS and HFS + S groups, although insulin levels in plasma and pancreas were unchanged. HFS induced expression of Srebp-1c, Glut1 and Ccl3 in adipose tissue, which were alleviated by selegiline. CONCLUSIONS AND IMPLICATIONS: Selegiline reduced adiposity, changes in adipose tissue energy metabolism and adipose inflammation induced by HFS diet without affecting the increased body weight, impairment of glucose homeostasis, or behaviour. These results suggest that selegiline could mitigate harmful effects of visceral adiposity.

Indexed as

Diet, High-FatAdipose Tissue, WhiteAdiposityAnimalsBlood PressureBody WeightChemokine CCL3Dietary SucroseEnergy IntakeGlucoseGlucose Transporter Type 1Lipid MetabolismMaleMembrane ProteinsMonoamine Oxidase InhibitorsOrgan SizeChemokine CCL3Dietary SucroseGlucoseGlucose Transporter Type 1Membrane ProteinsMonoamine Oxidase InhibitorsNdufa1 protein, mammalianSelegilineSlc2a1 protein, ratSrebf1 protein, ratSterol Regulatory Element Binding Protein 1

Identifiers

PMID29971762
PMCPMC6109222
OpenAlexW2811455148

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.