ArticleDiabetologia2014
The secretory deficit in islets from db/db mice is mainly due to a loss of responding beta cells.
Article in Diabetologia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 50 citations in OpenAlex.
- Dynamic Ca2+-Dependent Transcription Links Metabolic Stress to Impaired β-Cell Identity.Diabetes · 2025Article
- Partial remission of type 1 diabetes: Do immunometabolic events define the honeymoon period?Diabetes, obesity & metabolism · 2025Review
- Characteristics of Berberine Effects on Insulin Exocytosis in Pancreatic β Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Lessons from a model: early glucagon dysfunction in type 2 diabetes.Pflugers Archiv : European journal of physiology · 2025Article
- Strategy for the Identification of Host-Defense Peptides in Frog Skin Secretions with Therapeutic Potential as Antidiabetic Agents.Methods in molecular biology (Clifton, N.J.) · 2024Article
- CaFrontiers in endocrinology · 2024Review
- BRSK2 in pancreatic β cells promotes hyperinsulinemia-coupled insulin resistance and its genetic variants are associated with human type 2 diabetes.Journal of molecular cell biology · 2023Article
- Enhancement of Sphingomyelinase-Induced Endothelial Nitric Oxide Synthase-Mediated Vasorelaxation in a Murine Model of Type 2 Diabetes.International journal of molecular sciences · 2023Article
- The effect of forskolin and the role of Epac2A during activation, activity, and deactivation of beta cell networks.Frontiers in endocrinology · 2023Article
- pH-Dependence of Glucose-Dependent Activity of Beta Cell Networks in Acute Mouse Pancreatic Tissue Slice.Frontiers in endocrinology · 2022Article
- Caloric restriction recovers impaired β-cell-β-cell gap junction coupling, calcium oscillation coordination, and insulin secretion in prediabetic mice.American journal of physiology. Endocrinology and metabolism · 2020Article
- Acute insulin deprivation results in altered mitochondrial substrate sensitivity conducive to greater fatty acid transport.American journal of physiology. Endocrinology and metabolism · 2020Article
- Excitotoxicity and Overnutrition Additively Impair Metabolic Function and Identity of Pancreatic β-Cells.Diabetes · 2020Article
- Long-term c-Kit overexpression in beta cells compromises their function in ageing mice.Diabetologia · 2019Article
- Friend and foe: β-cell CaMolecular metabolism · 2019Review
- Pancreatic fibroblast growth factor 21 protects against type 2 diabetes in mice by promoting insulin expression and secretion in a PI3K/Akt signaling-dependent manner.Journal of cellular and molecular medicine · 2019Article
- Optical tools for understanding the complexity of β-cell signalling and insulin release.Nature reviews. Endocrinology · 2018Review
- The role of beta cell heterogeneity in islet function and insulin release.Journal of molecular endocrinology · 2018Review
- Synaptotagmin 4 Regulates Pancreatic β Cell Maturation by Modulating the CaDevelopmental cell · 2018Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisWe used the db/db mouse to determine the nature of the secretory defect in intact islets.
methodsGlucose tolerance was compared in db/db and wild-type (WT) mice. Isolated islets were used: to measure insulin secretion and calcium in a two-photon assay of single-insulin-granule fusion; and for immunofluorescence of soluble N-ethylmaleimide-sensitive factor attachment proteins (SNAREs).
resultsThe 13-18-week-old db/db mice showed a diabetic phenotype. Isolated db/db islets showed a 77% reduction in insulin secretion induced by 15 mmol/l glucose and reductions in the amplitude and rise-time of the calcium response to glucose. Ionomycin-induced insulin secretion in WT but not db/db islets. Immunofluorescence showed an increase in the levels of the SNAREs synaptosomal-associated protein 25 (SNAP25) and vesicle-associated membrane protein 2 (VAMP2) in db/db islets, but reduced syntaxin-1A. Therefore, db/db islets have both a compromised calcium response to glucose and a compromised secretory response to calcium. Two-photon microscopy of isolated islets determined the number and distribution of insulin granule exocytic events. Compared with WT, db/db islets showed far fewer exocytic events (an 83% decline at 15 mmol/l glucose). This decline was due to a 73% loss of responding cells and, in the remaining responsive cells, a 50% loss of exocytic responses per cell. An assay measuring granule re-acidification showed evidence for more recaptured granules in db/db islets compared with WT. CONCLUSIONS/
interpretationWe showed that db/db islets had a reduced calcium response to glucose and a reduction in syntaxin-1A. Within the db/db islets, changes were manifest as both a reduction in responding cells and a reduction in fusing insulin granules per cell.
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.