Evidence map›Paper›PMID 37432389›Full record

ReviewNutrients2023

Beta Cell Dysfunction in Youth- and Adult-Onset Type 2 Diabetes: An Extensive Narrative Review with a Special Focus on the Role of Nutrients.

Anastasios Serbis, Vasileios Giapros, Konstantinos Tsamis, Foteini Balomenou, Assimina Galli-Tsinopoulou, Ekaterini Siomou

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Nutrients, 2023. 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
6.7field-weighted citation impact, top 3% 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, 21 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Role of oxidative stress in prediabetes development.Biochemistry and biophysics reports · 2025
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
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 2 institutions in 1 country.

Anastasios SerbisDepartment of Pediatrics, School of Medicine, University of Ioannina, St. Niarhcos Avenue, 45500 Ioannina, Greece.ORCID 0000-0001-5422-3988
Vasileios GiaprosNeonatal Intensive Care Unit, School of Medicine, University of Ioannina, St. Νiarhcos Avenue, 45500 Ioannina, Greece.
Konstantinos TsamisDepartment of Physiology, Faculty of Medicine, School of Health Sciences, University of Ioannina, St. Niarhcos Avenue, 45500 Ioannina, Greece.ORCID 0000-0002-7032-1630
Foteini BalomenouNeonatal Intensive Care Unit, School of Medicine, University of Ioannina, St. Νiarhcos Avenue, 45500 Ioannina, Greece.
Assimina Galli-TsinopoulouSecond Department of Pediatrics, School of Medicine, Faculty of Health Sciences, Aristotle University of Thessaloniki, AHEPA University Hospital, Stilponos Kyriakidi 1, 54636 Thessaloniki, Greece.ORCID 0000-0002-8503-3893
Ekaterini SiomouDepartment of Pediatrics, School of Medicine, University of Ioannina, St. Niarhcos Avenue, 45500 Ioannina, Greece.
University of Ioannina · GRAristotle University of Thessaloniki · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traditionally a disease of adults, type 2 diabetes (T2D) has been increasingly diagnosed in youth, particularly among adolescents and young adults of minority ethnic groups. Especially, during the recent COVID-19 pandemic, obesity and prediabetes have surged not only in minority ethnic groups but also in the general population, further raising T2D risk. Regarding its pathogenesis, a gradually increasing insulin resistance due to central adiposity combined with a progressively defective β-cell function are the main culprits. Especially in youth-onset T2D, a rapid β-cell activity decline has been observed, leading to higher treatment failure rates, and early complications. In addition, it is well established that both the quantity and quality of food ingested by individuals play a key role in T2D pathogenesis. A chronic imbalance between caloric intake and expenditure together with impaired micronutrient intake can lead to obesity and insulin resistance on one hand, and β-cell failure and defective insulin production on the other. This review summarizes our evolving understanding of the pathophysiological mechanisms involved in defective insulin secretion by the pancreatic islets in youth- and adult-onset T2D and, further, of the role various micronutrients play in these pathomechanisms. This knowledge is essential if we are to curtail the serious long-term complications of T2D both in pediatric and adult populations.

Indexed as

Diabetes Mellitus, Type 2Insulin-Secreting CellsAdultAge of OnsetAnimalsEpigenesis, GeneticHumansInsulinNutrientsRisk FactorsInsulinNutrientsadolescentsinsulintype 2 diabetesyoung adultsyouthβ-cell failure

Identifiers

PMID37432389
PMCPMC10180650
OpenAlexW4381596869

What Socratic 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 Socratic graph.