ArticleDiabetologia2025
Intrapancreatic adipocytes and beta cell dedifferentiation in human type 2 diabetes.
Article in Diabetologia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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.
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.
Who cites it
12 citing papers in PubMed.
- Immunometabolism in Obesity-Associated Type 2 Diabetes: Molecular Mechanisms and Emerging Therapeutic Targets.International journal of molecular sciences · 2026Review
- The central role of the β-cell in diabetes: from monogenic forms to type 1, type 2, and gestational diabetes.Reviews in endocrine & metabolic disorders · 2026Review
- Mesenchymal Stem Cell-Derived Extracellular Vesicles Attenuate Diabetic β-Cell Apoptosis and Dedifferentiation by Delivering miR-4436.Tissue engineering and regenerative medicine · 2026Article
- Association of intra-pancreatic fat deposition with bone marrow adiposity in young obese adults.Quantitative imaging in medicine and surgery · 2026Article
- Conceptual framework and expert guidance on intrapancreatic fat deposition: the Melbourne consensus.Nature reviews. Gastroenterology & hepatology · 2026Review
- Fatty Pancreas and Risk of Type 2 Diabetes, Chronic Kidney Disease and Cardiovascular Events: Evidence From a Population-Based Cohort.United European gastroenterology journal · 2026Article
- Single-cell RNA-seq and in vitro study reveal Fusobacterium nucleatum impairs β-cell identity in type 2 diabetes via the NF-κB-CDKN1C axis.Journal of translational medicine · 2026Article
- Explainable AI-based analysis of human pancreas sections identifies traits of type 2 diabetes.Nature communications · 2026Article
- The Natural History of Prediabetes and Cardiovascular Disease in the Pediatric Population.Biomedicines · 2026Review
- The Fatty Pancreas: Current Evidence, Treatment Implications, and Future Directions.Gastro hep advances · 2026Review
- Quantitative pancreatic MRI in diabetes mellitus: current advances and future directions.Frontiers in endocrinology · 2026Review
- Loss of β-cell identity in human islets treated with glibenclamide.Diabetes, obesity & metabolism · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
aims/hypothesisFat deposition in the pancreas is implicated in beta cell dysfunction and the progress of type 2 diabetes. However, there is limited evidence to confirm the correlation and explore how pancreatic fat links with beta cell dysfunction in human type 2 diabetes. This study aimed to examine the spatial relationship between pancreatic fat and islets in human pancreases.
methodsHistological analysis of pancreatic specimens from 50 organ donors (15 with type 2 diabetes, 35 without) assessed pancreatic fat content variation among individuals with diabetes and its correlation with estimated beta cell mass and cell distribution within islets. Bioinformatic analysis of single-cell RNA-seq of 11 type 2 diabetic donors (from the Human Pancreatic Analysis Project database) explored the impact of high pancreatic fat content on beta cell gene expression and cell fate. Validation of bioinformatic results was performed with the above diabetic pancreases.
resultsPancreatic fat content was higher in individuals with type 2 diabetes (10.24% [3.29-13.89%] vs 0.74% [0.34-5.11%], p<0.001), negatively correlated with estimated beta cell mass (r=-0.675, p=0.006) and positively with alpha-to-beta cell ratio (r=0.608, p=0.016). Enrichment analysis indicated that in diabetic donors with higher pancreatic fat content, the expression of ALDH1A3, beta cell dedifferentiation marker, in both alpha and beta cells was significantly increased, and in beta cells, the expression of NPY decreased. Pseudotime analysis revealed beta cell dedifferentiation and transdifferentiation towards alpha cells in diabetic donors with higher pancreatic fat content, with decreased expression of genes related to beta cell maturation and function, including INSM1, MafA and NPY. Concurrently, pathways related to inflammation and immune response were activated. Histologically, pancreatic fat content correlated positively with the percentage of beta cells positive for aldehyde dehydrogenase 1 family member A3 (ALDH1A3) within the islets (r=0.594, p=0.020) and the ALDH1A3 positivity rate in beta cells (r=0.615, p=0.015). And the number of T cells adjacent to adipocytes was related to the distribution pattern of adipocytes and the dedifferentiation phenotype in islets. CONCLUSIONS/
interpretationHigher pancreatic fat content was accompanied by increased beta cell dedifferentiation in the individuals with diabetes. Clusters of adipocytes significantly contribute to higher pancreatic fat content and immune cell recruitment. Overall, the interactions among adipocytes, immune cells and beta cells in the pancreas microenvironment might contribute to beta cell failure and dedifferentiation in type 2 diabetes.
Indexed as
Identifiers
40072535What Socratic holds
Registered trials
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.