ReviewEndocrinology2021
The Pancreatic ß-cell Response to Secretory Demands and Adaption to Stress.
Review in Endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed.
- Determination of Expression and Relationships of Nedd4-Related E3 Ubiquitin Ligase-2 (NEDL2) and Ubiquitin Proteasome System Proteins in Developing Rat Pancreatic Tissue.Anatomia, histologia, embryologia · 2026Article
- Molecular Mechanisms Associated with Metabolic Dysfunction: Contributions of Nutritional Genomics.Metabolites · 2026Review
- Article
- Article
- Stimulation to secrete insulin induces pancreatic β-cell dysfunction through Tfe3 activation.iScience · 2026Article
- Chestnut-derived ellagitannins (FT50) protect against western diet-induced metabolic dysfunction and preserve beta cell function in mice.Frontiers in endocrinology · 2026Article
- Mechanistic insights into cargo sorting and export from the Golgi apparatus.Nature reviews. Molecular cell biology · 2025Review
- Metabolic challenges of glucose and lipid dysregulation in psoriatic arthritis: a narrative review from pathogenesis to clinical practice.Acta diabetologica · 2025Review
- IL-1β priming triggers an adaptive stress response that enhances pancreatic β-cell resilience to subsequent cytotoxic inflammatory insult.Cell death & disease · 2025Article
- Article
- Unique and conserved endoplasmic reticulum stress responses in neuroendocrine cells.bioRxiv : the preprint server for biology · 2025Article
- Dynamic Ca2+-Dependent Transcription Links Metabolic Stress to Impaired β-Cell Identity.Diabetes · 2025Article
- Trapα deficiency impairs the early events of insulin biosynthesis and glucose homeostasis.The Journal of clinical investigation · 2025Article
- VDAC1 is a target for pharmacologically induced insulin hypersecretion in β cells.Cell reports · 2025Article
- Myricetin Amplifies Glucose-Stimulated Insulin Secretion via the cAMP-PKA-Epac-2 Signaling Cascade.Biomedicines · 2025Article
- Insulin Resistance in Type 1 Diabetes: Pathophysiological, Clinical, and Therapeutic Relevance.Endocrine reviews · 2025Review
- Harnessing beta-cell replication: advancing molecular insights to regenerative therapies in diabetes.Frontiers in endocrinology · 2025Review
- CaFrontiers in endocrinology · 2024Review
- Whole Exome Sequencing in Children With Type 1 Diabetes Before Age 6 Years Reveals Insights Into Disease Heterogeneity.Journal of diabetes research · 2024Article
- What is the role of puberty in the development of islet autoimmunity and progression to type 1 diabetes?European journal of epidemiology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Pancreatic β cells dedicate much of their protein translation capacity to producing insulin to maintain glucose homeostasis. In response to increased secretory demand, β cells can compensate by increasing insulin production capability even in the face of protracted peripheral insulin resistance. The ability to amplify insulin secretion in response to hyperglycemia is a critical facet of β-cell function, and the exact mechanisms by which this occurs have been studied for decades. To adapt to the constant and fast-changing demands for insulin production, β cells use the unfolded protein response of the endoplasmic reticulum. Failure of these compensatory mechanisms contributes to both type 1 and 2 diabetes. Additionally, studies in which β cells are "rested" by reducing endogenous insulin demand have shown promise as a therapeutic strategy that could be applied more broadly. Here, we review recent findings in β cells pertaining to the metabolic amplifying pathway, the unfolded protein response, and potential advances in therapeutics based on β-cell rest.
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.