Evidence map›Paper›PMID 34879109›Full record

ArticlePloS one2021

Protective role of melatonin against adipose-hepatic metabolic comorbidities in experimentally induced obese rat model.

Mary J Obayemi, Christopher O Akintayo, Adesola A Oniyide, Ayodeji Aturamu, Olabimpe C Badejogbin, Chukwubueze L Atuma, Azeezat O Saidi, Hadiza Mahmud, Kehinde S Olaniyi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed, 14 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

9 authors at 2 institutions in 1 country.

Mary J ObayemiDepartment of Physiology, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Nigeria.
Christopher O AkintayoDepartment of Physiology, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Nigeria.
Adesola A OniyideDepartment of Physiology, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Nigeria.
Ayodeji AturamuDepartment of Physiology, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Nigeria.
Olabimpe C BadejogbinDepartment of Physiology, Benjamin Carson School of Medicine, Babcock University, Ilishan-Remo, Nigeria.
Chukwubueze L AtumaDepartment of Physiology, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Nigeria.
Azeezat O SaidiDepartment of Physiology, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Nigeria.
Hadiza MahmudDepartment of Physiology, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Nigeria.
Kehinde S OlaniyiDepartment of Physiology, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Nigeria.ORCID 0000-0002-8229-9688
Afe Babalola University · NGBabcock University · NG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAdipose and hepatic metabolic dysfunctions are critical comorbidities that also aggravate insulin resistance in obese individuals. Melatonin is a low-cost agent and previous studies suggest that its use may promote metabolic health. However, its effects on some comorbidities associated with obesity are unknown. Herein, we investigated the hypothesis that melatonin supplementation would attenuate adipose-hepatic metabolic dysfunction in high fat diet (HFD)-induced obesity in male Wistar rats. MATERIALS AND

methodsTwenty-four adult male Wistar rats (n = 6/group) were used: Control group received vehicle (normal saline), obese group received 40% high fat diet, melatonin-treated group received 4 mg/kg of melatonin, and obese plus melatonin group received 40% HFD and melatonin. The treatment lasted for 12 weeks.

resultsHFD caused increased food intake, body weight, insulin level, insulin resistance and plasma and liver lipid but decreased adipose lipid. In addition, HFD also increased plasma, adipose and liver malondialdehyde, IL-6, uric acid and decreased Glucose-6-phosphate dehydrogenase, glutathione, nitric oxide and circulating obestatin concentration. However, these deleterious effects except food intake were attenuated when supplemented with melatonin.

conclusionTaken together, the present results indicate that HFD exposure causes adipose-hepatic metabolic disturbance in obese animals, which are accompanied by oxidative stress and inflammation. In addition, the present results suggest that melatonin supplementation attenuates adipose-hepatic metabolic dysfunction, accompanying obesity by suppression of oxidative stress/inflammation-dependent mechanism and increasing circulating obestatin.

Indexed as

Adipose TissueAnimalsDiet, High-FatDisease Models, AnimalGene Expression RegulationGhrelinGlucosephosphate DehydrogenaseInterleukin-6LiverMaleMalondialdehydeMelatoninNitric OxideObesityRatsRats, WistarGhrelinGlucosephosphate DehydrogenaseIL6 protein, humanInterleukin-6MalondialdehydeMelatoninNitric Oxideobestatin, humanUric Acid

Identifiers

PMID34879109
PMCPMC8654266
OpenAlexW4200412487

What OpenQuestion holds

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LicenceCC BY
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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.