Evidence map›Paper›PMID 36686442›Full record

ReviewFrontiers in endocrinology2022

Asprosin in health and disease, a new glucose sensor with central and peripheral metabolic effects.

Mariam Farrag, Djedjiga Ait Eldjoudi, María González-Rodríguez, Alfonso Cordero-Barreal, Clara Ruiz-Fernández, Maurizio Capuozzo, Miguel Angel González-Gay, Antonio Mera, Francisca Lago, Ahmed Soffar and 4 more

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
10.9field-weighted citation impact, top 1% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Article
  8. Observational
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Observational
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

14 authors at 5 institutions in 2 countries.

Mariam FarragSERGAS (Servizo Galego de Saude), NEIRID Lab (Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases), Research Laboratory 9, IDIS (Instituto de Investigación Sanitaria de Santiago), Santiago University Clinical Hospital, Santiago de Compostela, Spain.
Djedjiga Ait EldjoudiSERGAS (Servizo Galego de Saude), NEIRID Lab (Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases), Research Laboratory 9, IDIS (Instituto de Investigación Sanitaria de Santiago), Santiago University Clinical Hospital, Santiago de Compostela, Spain.
María González-RodríguezSERGAS (Servizo Galego de Saude), NEIRID Lab (Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases), Research Laboratory 9, IDIS (Instituto de Investigación Sanitaria de Santiago), Santiago University Clinical Hospital, Santiago de Compostela, Spain.
Alfonso Cordero-BarrealSERGAS (Servizo Galego de Saude), NEIRID Lab (Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases), Research Laboratory 9, IDIS (Instituto de Investigación Sanitaria de Santiago), Santiago University Clinical Hospital, Santiago de Compostela, Spain.
Clara Ruiz-FernándezSERGAS (Servizo Galego de Saude), NEIRID Lab (Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases), Research Laboratory 9, IDIS (Instituto de Investigación Sanitaria de Santiago), Santiago University Clinical Hospital, Santiago de Compostela, Spain.
Maurizio CapuozzoNational Health Service, Local Health Authority ASL 3 Napoli Sud, Department of Pharmacy, Naples, Italy.
Miguel Angel González-GayHospital Universitario Marqués de Valdecilla, Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IDIVAL, University of Cantabria, Santander, Cantabria, Spain.
Antonio MeraSERGAS, Santiago University Clinical Hospital, Division of Rheumatology, Santiago de Compostela, Spain.
Francisca LagoSERGAS (Servizo Galego de Saude), IDIS (Instituto de Investigación Sanitaria de Santiago), Molecular and Cellular Cardiology Lab, Research Laboratory 7, Santiago University Clinical Hospital, Santiago de Compostela, Spain.
Ahmed SoffarFaculty of Science, Alexandria University, Alexandria, Egypt.
Amina EssawyFaculty of Science, Alexandria University, Alexandria, Egypt.
Jesus PinoSERGAS (Servizo Galego de Saude), NEIRID Lab (Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases), Research Laboratory 9, IDIS (Instituto de Investigación Sanitaria de Santiago), Santiago University Clinical Hospital, Santiago de Compostela, Spain.
Yousof FarragSERGAS (Servizo Galego de Saude), NEIRID Lab (Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases), Research Laboratory 9, IDIS (Instituto de Investigación Sanitaria de Santiago), Santiago University Clinical Hospital, Santiago de Compostela, Spain.
Oreste GualilloSERGAS (Servizo Galego de Saude), NEIRID Lab (Neuroendocrine Interactions in Rheumatology and Inflammatory Diseases), Research Laboratory 9, IDIS (Instituto de Investigación Sanitaria de Santiago), Santiago University Clinical Hospital, Santiago de Compostela, Spain.
Servicio Gallego de Salud · ESInstituto de Investigación Sanitaria de Santiago · ESAlexandria University · EGUniversidad de Cantabria · ESUniversidade de Santiago de Compostela · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adipose tissue malfunction leads to altered adipokine secretion which might consequently contribute to an array of metabolic diseases spectrum including obesity, diabetes mellitus, and cardiovascular disorders. Asprosin is a novel diabetogenic adipokine classified as a caudamin hormone protein. This adipokine is released from white adipose tissue during fasting and elicits glucogenic and orexigenic effects. Although white adipose tissue is the dominant source for this multitask adipokine, other tissues also may produce asprosin such as salivary glands, pancreatic B-cells, and cartilage. Significantly, plasma asprosin levels link to glucose metabolism, lipid profile, insulin resistance (IR), and β-cell function. Indeed, asprosin exhibits a potent role in the metabolic process, induces hepatic glucose production, and influences appetite behavior. Clinical and preclinical research showed dysregulated levels of circulating asprosin in several metabolic diseases including obesity, type 2 diabetes mellitus (T2DM), polycystic ovarian syndrome (PCOS), non-alcoholic fatty liver (NAFLD), and several types of cancer. This review provides a comprehensive overview of the asprosin role in the etiology and pathophysiological manifestations of these conditions. Asprosin could be a promising candidate for both novel pharmacological treatment strategies and diagnostic tools, although developing a better understanding of its function and signaling pathways is still needed.

Indexed as

Diabetes Mellitus, Type 2Peptide HormonesAdipokinesFemaleGlucoseHumansObesityAdipokinesGlucosePeptide Hormonesadipokinesasprosindiabetesmetabolic diseasesobesityPCOS

Identifiers

PMID36686442
PMCPMC9849689
OpenAlexW4313509552

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.