Evidence map›Paper›PMID 40591035›Full record

ArticleActa diabetologica2025

Unmasking heterogeneity in type 2 diabetes: the clinical relevance of phenotyping in the era of precision medicine.

Salvatore Corrao, Massimo Federici

Abstract read
PubMed Publisher
In one paragraph

Article in Acta diabetologica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. 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

2 authors.

Salvatore CorraoDepartment of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (PROMISE), University of Palermo, Palermo, Italy. salvatore.corrao@unipa.it.ORCID http://orcid.org/0000-0001-5621-1374
Massimo FedericiDepartment of Systems Medicine, University of Rome Tor Vergata, Rome, Italy.ORCID http://orcid.org/0000-0003-4989-5194

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite its widespread use in clinical practice, the traditional dichotomous classification of diabetes into type 1 and type 2 fails to capture the marked heterogeneity observed in real-world patients, particularly those with type 2 diabetes mellitus (T2DM). The increasing recognition of the complex interplay between insulin resistance, beta-cell dysfunction, autoimmunity, and genetic predisposition has led to the development of phenotypic classification systems that aim to individualize care beyond glycemic targets. Ahlqvist et al. made a major contribution to this field by identifying five clinically meaningful clusters of adult-onset diabetes using routine clinical variables. These clusters differ in their metabolic profiles, complication risks, and therapeutic needs, offering a pragmatic starting point for personalized diabetology. Their clinical relevance has been further explored and validated by follow-up studies that include detailed metabolic phenotyping, cardiac imaging, and genetic analyses. Nevertheless, enthusiasm for cluster-based models must be tempered by critical appraisal. Evidence from large trials suggests that continuous clinical features may better predict disease progression and treatment response than static cluster assignments. Furthermore, these models have yet to be integrated into clinical guidelines or electronic decision-support systems. This Perspective argues for a multidimensional and dynamic approach to diabetes phenotyping, combining clinical, biochemical, imaging, and genetic data to reflect the evolving nature of the disease. Such a framework could enable more precise stratification and intervention, moving toward truly personalized diabetes care. Integrating these models into real-world settings represents the next frontier in precision diabetology.

Indexed as

Diabetes Mellitus, Type 2Precision MedicineClinical RelevanceHumansInsulin ResistancePhenotypeBeta-cell functionCardiometabolic riskCluster analysisDiabetes phenotypingDiabetes subgroupsInsulin resistancePersonalized therapyPrecision medicine

Identifiers

PMID40591035

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.