ArticleFrontiers in endocrinology2013
Beta cell dysfunction and insulin resistance.
Article in Frontiers in endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 418 papers, 7 of them syntheses that pooled it.
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Who cites it
418 citing papers in PubMed, 7 syntheses or guidelines pooled it.
- From Molecules to Biomarkers: Nogo Proteins and Receptors in the Early Detection of Type 2 Diabetes Complications: A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Key biomarkers in type 2 diabetes patients: A systematic review.Diabetes, obesity & metabolism · 2025Pooled it
- Pooled it
- Prevalence of new-onset diabetes mellitus after kidney transplantation: a systematic review and meta-analysis.Acta diabetologica · 2024Pooled it
- Association between prediabetes and breast cancer: a comprehensive meta-analysis.Breast cancer research and treatment · 2024Pooled it
- Vitamin D deficiency and its associated factors among patients with type 2 diabetes mellitus: a systematic review and meta-analysis.BMJ open · 2023Pooled it
- Host insulin resistance caused byFrontiers in cellular and infection microbiology · 2023Pooled it
- Comparison of protective effects of teneligliptin and luseogliflozin on pancreatic β-cell function: randomized, parallel-group, multicenter, open-label study (SECRETE-I study).Frontiers in endocrinology · 2024Trial
- Efficacy of multigrain supplementation in type 2 diabetes mellitus: A pilot study protocol for a randomized intervention trial.World journal of diabetes · 2023Trial
- A functional missense variant iniScience · 2026Article
- Hyperglycemia associated brain dysfunction: rodent models for studying diabetic cognitive deficits.Metabolic brain disease · 2026Review
- Conditional eIF2A Deletion Suggests Extra-Adipose Mechanisms Underlying Metabolic Syndrome in Total-Body eIF2A Knockout Mice.FASEB bioAdvances · 2026Article
- Empagliflozin inhibits the apoptosis of pancreatic β-cells through amelioration of endoplasmic reticulum (ER) stress.Metabolism open · 2026Article
- Intra-Islet Paracrine Regulation of Glucagon Secretion During Hypoglycemia, Euglycemia, and Hyperglycemia.Annals of the New York Academy of Sciences · 2026Review
- Liposomal Delivery ofPharmaceutics · 2026Article
- A Review of Semi-Mechanistic HbA1c Models in People with Type 2 Diabetes: Strengths, Limitations, and Applications.Journal of clinical pharmacology · 2026Review
- Heterogeneous expression patterns of the T2D-associated kinesin-4 KIF21A in pancreatic islet endocrine cells.Molecular metabolism · 2026Article
- Therapeutic potential of spexin in diabetic neuropathy: Insights from in vitro and in vivo models.Experimental physiology · 2026Article
- The bile acid-sensive ion channel (BASIC) is expressed in pancreatic α-cells and involved in glucagon secretion.Pflugers Archiv : European journal of physiology · 2026Review
- Design, Synthesis,Molecules (Basel, Switzerland) · 2026Article
358 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Beta cell dysfunction and insulin resistance are inherently complex with their interrelation for triggering the pathogenesis of diabetes also somewhat undefined. Both pathogenic states induce hyperglycemia and therefore increase insulin demand. Beta cell dysfunction results from inadequate glucose sensing to stimulate insulin secretion therefore elevated glucose concentrations prevail. Persistently elevated glucose concentrations above the physiological range result in the manifestation of hyperglycemia. With systemic insulin resistance, insulin signaling within glucose recipient tissues is defective therefore hyperglycemia perseveres. Beta cell dysfunction supersedes insulin resistance in inducing diabetes. Both pathological states influence each other and presumably synergistically exacerbate diabetes. Preserving beta cell function and insulin signaling in beta cells and insulin signaling in the glucose recipient tissues will maintain glucose homeostasis.
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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.