Evidence map›Paper›PMID 36612350›Full record

ReviewInternational journal of environmental research and public health2022

Circadian Clock Desynchronization and Insulin Resistance.

Federica Catalano, Francesca De Vito, Velia Cassano, Teresa Vanessa Fiorentino, Angela Sciacqua, Marta Letizia Hribal

Abstract readReview
In one paragraph

Review in International journal of environmental research and public health, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Observational
  5. Article
  6. Article
  7. Review
  8. Review
  9. Artificial Light at Night and Type 2 Diabetes Mellitus.Diabetes & metabolism journal · 2024
    Review
  10. Article
  11. Review
  12. Review
  13. Review
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.

Federica CatalanoDepartment of Medical and Surgical Sciences, University of Catanzaro "Magna Graecia", 88100 Catanzaro, Italy.
Francesca De VitoDepartment of Medical and Surgical Sciences, University of Catanzaro "Magna Graecia", 88100 Catanzaro, Italy.
Velia CassanoDepartment of Medical and Surgical Sciences, University of Catanzaro "Magna Graecia", 88100 Catanzaro, Italy.
Teresa Vanessa FiorentinoDepartment of Medical and Surgical Sciences, University of Catanzaro "Magna Graecia", 88100 Catanzaro, Italy.
Angela SciacquaDepartment of Medical and Surgical Sciences, University of Catanzaro "Magna Graecia", 88100 Catanzaro, Italy.
Marta Letizia HribalDepartment of Medical and Surgical Sciences, University of Catanzaro "Magna Graecia", 88100 Catanzaro, Italy.ORCID 0000-0001-5932-0541

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The circadian rhythm regulates biological processes that occur within 24 h in living organisms. It plays a fundamental role in maintaining biological functions and responds to several inputs, including food intake, light/dark cycle, sleep/wake cycle, and physical activity. The circadian timing system comprises a central clock located in the suprachiasmatic nucleus (SCN) and tissue-specific clocks in peripheral tissues. Several studies show that the desynchronization of central and peripheral clocks is associated with an increased incidence of insulin resistance (IR) and related diseases. In this review, we discuss the current knowledge of molecular and cellular mechanisms underlying the impact of circadian clock dysregulation on insulin action. We focus our attention on two possible mediators of this interaction: the phosphatases belonging to the pleckstrin homology leucine-rich repeat protein phosphatase family (PHLPP) family and the deacetylase Sirtuin1. We believe that literature data, herein summarized, suggest that a thorough change of life habits, with the return to synchronized food intake, physical activity, and rest, would doubtless halt the vicious cycle linking IR to dysregulated circadian rhythms. However, since such a comprehensive change may be incompatible with the demand of modern society, clarifying the pathways involved may, nonetheless, contribute to the identification of therapeutic targets that may be exploited to cure or prevent IR-related diseases.

Indexed as

Circadian ClocksInsulin ResistanceCircadian RhythmHumansPhotoperiodSuprachiasmatic Nucleuscircadian clockinsulin sensitivityinsulin signalingperipheral tissues

Identifiers

PMID36612350
PMCPMC9819930

What OpenQuestion holds

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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.