Evidence map›Paper›PMID 37874505›Full record

SynthesisMolecular biology reports2023

The cross-talk between leptin and circadian rhythm signaling proteins in physiological processes: a systematic review.

Atefeh Ansarin, Aida Malek Mahdavi, Zeinab Javadivala, Dariush Shanehbandi, Habib Zarredar, Khalil Ansarin

Abstract readSystematic Review
PubMed Publisher
In one paragraph

Synthesis in Molecular biology reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 15% 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, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
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  7. 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

6 authors at 1 institution in 1 country.

Atefeh AnsarinTuberculosis and Lung Disease Research Center, Tabriz University of Medical Sciences, Pashmineh Research Complex, Daneshgah Street, P.O. Box: 5448151429, Tabriz, Iran.
Aida Malek MahdaviTuberculosis and Lung Disease Research Center, Tabriz University of Medical Sciences, Pashmineh Research Complex, Daneshgah Street, P.O. Box: 5448151429, Tabriz, Iran.
Zeinab JavadivalaDepartment of Health Education & Promotion, Tabriz University of Medical Sciences, Tabriz, Iran.
Dariush ShanehbandiImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Habib ZarredarTuberculosis and Lung Disease Research Center, Tabriz University of Medical Sciences, Pashmineh Research Complex, Daneshgah Street, P.O. Box: 5448151429, Tabriz, Iran.
Khalil AnsarinTuberculosis and Lung Disease Research Center, Tabriz University of Medical Sciences, Pashmineh Research Complex, Daneshgah Street, P.O. Box: 5448151429, Tabriz, Iran. ansarink@tbzmed.ac.ir.
Tabriz University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundToday, modern lifestyles and disrupted sleep patterns cause circadian clock rhythm impairments that are associated with altered leptin levels, which subsequently affect a wide range of physiological processes and have significant health burdens on societies. Nevertheless, there has been no systematic review of circadian clock genes and proteins, leptin, and related signaling pathways.

methodsAccordingly, we systematically reviewed circadian clock proteins, leptin, and molecular mechanisms between them by searching Pubmed, Scopus, ProQuest, Web of Sciences, and Google Scholar until September 2022. After considering the inclusion and exclusion criteria, 20 animal studies were selected. The risk of bias was assessed in each study.

resultsThe results clarified the reciprocal interconnected relationship between circadian clock genes and leptin. Circadian clock genes regulate leptin expression and signaling via different mechanisms, such as CLOCK-BMAL1 heterodimers, which increase the expression of PPARs. PPARs induce the expression of C/EBPα, a key factor in upregulating leptin expression. CLOCK-BMAL1 also induces the expression of Per1 and Rev-erb genes. PER1 activates mTORC1 and mTORC1 enhances the expression of C/EBPα. In addition, REV-ERBs activate the leptin signaling pathway. Also, leptin controls the expression of circadian clock genes by triggering the AMPK and ERK/MAPK signaling pathways, which regulate the activity of PPARs. Moreover, the roles of these molecular mechanisms are elucidated in different physiological processes and organs.

conclusionsCrosstalk between circadian clock genes and leptin and their affecting elements should be considered in the selection of new therapeutic targets for related disorders, especially obesity and metabolic impairments.

Indexed as

Circadian ClocksCircadian Rhythm Signaling Peptides and ProteinsAnimalsARNTL Transcription FactorsCircadian RhythmHumansLeptinMechanistic Target of Rapamycin Complex 1Nuclear Receptor Subfamily 1, Group D, Member 1Peroxisome Proliferator-Activated ReceptorsARNTL Transcription FactorsCircadian Rhythm Signaling Peptides and ProteinsLEP protein, humanLeptinMechanistic Target of Rapamycin Complex 1Nuclear Receptor Subfamily 1, Group D, Member 1Peroxisome Proliferator-Activated ReceptorsBMAL1Circadian rhythmClock genesLeptinMetabolismREV-ERBα

Identifiers

PMID37874505
OpenAlexW4387893291

What OpenQuestion holds

Textmetadata
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.