ReviewMolecular endocrinology (Baltimore, Md.)2009
Minireview: Meeting the demand for insulin: molecular mechanisms of adaptive postnatal beta-cell mass expansion.
Review in Molecular endocrinology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 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
95 citing papers in PubMed, 156 citations in OpenAlex.
- BAF60A governs beta cell identity to control systemic glucose homeostasis.Diabetologia · 2026Article
- Toll-like receptor 2 modulates age-associated insulitis and fibrotic remodeling of Langerhans islets.Immunity & ageing : I & A · 2026Article
- Article
- Duodenal neuroendocrine cells and neuromedin U in subjects with obesity: Relationship with type 2 diabetes and glucose homeostasis.Physiological reports · 2025Article
- Retrograde mitochondrial signaling governs the identity and maturity of metabolic tissues.Science (New York, N.Y.) · 2025Article
- Application of Ultrasound Localization Microscopy in Evaluating the Type 2 Diabetes Progression.Cyborg and bionic systems (Washington, D.C.) · 2025Article
- Enhancing insulin secretion by pancreatic β-cell redifferentiation: a study of the anti-diabetic effects of berberineFrontiers in endocrinology · 2025Article
- Partial Deletion of Perk Improved High-Fat Diet-Induced Glucose Intolerance in Mice.Endocrinology and metabolism (Seoul, Korea) · 2023Article
- Beta-cell compensation and gestational diabetes.The Journal of biological chemistry · 2023Review
- Review
- Endocrine disruptors in plastics alter β-cell physiology and increase the risk of diabetes mellitus.American journal of physiology. Endocrinology and metabolism · 2023Review
- Dopamine receptor agonists mechanism of actions on glucose lowering and their connections with prolactin actions.Frontiers in clinical diabetes and healthcare · 2023Review
- Therapeutic Strategies Targeting Pancreatic Islet β-Cell Proliferation, Regeneration, and Replacement.Endocrinology · 2022Article
- Acetone Ingestion Mimics a Fasting State to Improve Glucose Tolerance in a Mouse Model of Gestational Hyperglycemia.International journal of molecular sciences · 2021Article
- β-Arrestin-1 is required for adaptive β-cell mass expansion during obesity.Nature communications · 2021Article
- Autocrine IGF2 programmes β-cell plasticity under conditions of increased metabolic demand.Scientific reports · 2021Article
- Increased alpha and beta cell mass during mouse pregnancy is not dependent on transdifferentiation.Experimental biology and medicine (Maywood, N.J.) · 2021Article
- 5-Bromoprotocatechualdehyde Combats against Palmitate Toxicity by Inhibiting Parkin Degradation and Reducing ROS-Induced Mitochondrial Damage in Pancreatic β-Cells.Antioxidants (Basel, Switzerland) · 2021Article
- An Autonomous Cannabinoid System in Islets of Langerhans.Frontiers in endocrinology · 2021Review
- Monoclonal therapy against calcitonin gene-related peptide lowers hyperglycemia and adiposity in type 2 diabetes mouse models.Metabolism open · 2020Article
35 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Type 2 diabetes results from pancreatic ss-cell failure in the setting of insulin resistance. This model of disease progression has received recent support from the results of genome-wide association studies that identify genes potentially regulating ss-cell growth and function as type 2 diabetes susceptibility loci. Normal ss-cell compensation for an increased insulin demand includes both enhanced insulin-secretory capacity and an expansion of morphological ss-cell mass, due largely to changes in the balance between ss-cell proliferation and apoptosis. Recent years have brought significant progress in the understanding of both extrinsic signals stimulating ss-cell growth as well as mediators intrinsic to the ss-cell that regulate the compensatory response. Here, we review the current knowledge of mechanisms underlying adaptive expansion of ss-cell mass, focusing on lessons learned from experimental models of physiologically occurring insulin-resistant states including diet-induced obesity and pregnancy, and highlighting the potential importance of interorgan cross talk. The identification of critical mediators of islet compensation may direct the development of future therapeutic strategies to enhance the response of ss-cells to insulin resistance.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.