ReviewThe lancet. Diabetes & endocrinology2020
Inadequate β-cell mass is essential for the pathogenesis of type 2 diabetes.
Review in The lancet. Diabetes & endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
103 citing papers in PubMed, 2 syntheses or guidelines pooled it, 189 citations in OpenAlex.
- Pooled it
- Interventions for preventing type 2 diabetes in adults with mental disorders in low- and middle-income countries.The Cochrane database of systematic reviews · 2021 · on this mapPooled it
- Efficacy and Safety of Triple Fixed Dose Combination of Dapagliflozin + Sitagliptin + Metformin IR in Indian Patients with Type 2 Diabetes Mellitus: A Randomized, Phase 3 Study in Comparison with Dual FDC Sitagliptin + Metformin IR.Advances in therapy · 2025Trial
- Insulin Secretion Predicts the Response to Antidiabetic Therapy in Patients With New-onset Diabetes.The Journal of clinical endocrinology and metabolism · 2021Trial
- Pancreaticoduodenectomy model demonstrates a fundamental role of dysfunctional β cells in predicting diabetes.The Journal of clinical investigation · 2021Trial
- Durability of Triple Combination Therapy Versus Stepwise Addition Therapy in Patients With New-Onset T2DM: 3-Year Follow-up of EDICT.Diabetes care · 2021 · on this mapTrial
- Regulation of pancreatic beta-cell mass and its importance for antidiabetic therapies.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Plasma small RNA profiling reveals a three-miRNA signature associated with early beta cell dysfunction across glucose tolerance stages.Diabetologia · 2026Article
- Temporal single-cell transcriptional dynamics of murine pancreatic islet remodeling during hyperglycaemia progression.Molecular metabolism · 2026Article
- The Potential Physiologic Mechanisms by Which Early-Life Nutrition May Influence Type 2 Diabetes Pathophysiology in Humans.Annual review of nutrition · 2026Review
- Unraveling A-β+ ketosis-prone diabetes: An evolving diagnosis with an elusive pathogenesis.Journal of diabetes investigation · 2026Review
- Explainable AI-based analysis of human pancreas sections identifies traits of type 2 diabetes.Nature communications · 2026Article
- Volume and functional changes of remnant pancreas after different types of pancreatectomy: Exploring the regenerative potential.Scientific reports · 2026Article
- The Impact of the Multidisciplinary Team on Medication Adherence in Type 2 Diabetes: A Narrative Review.Journal of multidisciplinary healthcare · 2026Review
- Article
- Article
- Identification of type 2 diabetes- and obesity-associated human β-cells using deep transfer learning.eLife · 2025Article
- Ras homolog enriched in brain 1 regulates β cell mass and β cell functionWorld journal of diabetes · 2025Article
- The role of the farnesoid X receptor in diabetes and its complications.Molecular and cellular biochemistry · 2025Review
- Shenqi compound enhances pancreatic β-cell secretion by promoting the maturation and transport of insulin secretory vesicles through the NOD1/RIP2 signaling pathway.Frontiers in nutrition · 2025Article
43 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
For patients with type 1 diabetes, it is accepted among the scientific community that there is a marked reduction in β-cell mass; however, with type 2 diabetes, there is disagreement as to whether this reduction in mass occurs in every case. Some have argued that β-cell mass in some patients with type 2 diabetes is normal and that the cause of the hyperglycaemia in these patients is a functional abnormality of insulin secretion. In this Personal View, we argue that a deficient β-cell mass is essential for the development of type 2 diabetes. The main point is that there are enormous (≥10 fold) variations in insulin sensitivity and insulin secretion in the general population, with a very close correlation between these two factors for any individual. Although β-cell mass cannot be accurately measured in living patients, it is highly likely that it too is highly correlated with insulin sensitivity and secretion. Thus, our argument is that a person with type 2 diabetes can have a β-cell mass that is the same as a person without type 2 diabetes, but because they are insulin resistant, the mass is inadequate and responsible for their diabetes. Because the abnormal insulin secretion of diabetes is caused by dysglycaemia and can be largely reversed with glycaemic control, it is a less serious problem than the reduction in β-cell mass, which is far more difficult to restore.
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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 OpenQuestion graph.