ArticleThe Journal of general physiology2007
Ca2+-secretion coupling is impaired in diabetic Goto Kakizaki rats.
Article in The Journal of general physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 60 citations in OpenAlex.
- TALK-1-mediated alterations of β-cell mitochondrial function and insulin secretion impair glucose homeostasis on a diabetogenic diet.Cell reports · 2024Article
- Bridging the Gap: Pancreas Tissue Slices From Organ and Tissue Donors for the Study of Diabetes Pathogenesis.Diabetes · 2024Review
- CaBiomedicines · 2023Review
- In Vivo CaBiomedicines · 2023Article
- High-resolution analysis of the cytosolic CaAmerican journal of physiology. Endocrinology and metabolism · 2023Article
- Article
- Mitochondrial Heterogeneity in Metabolic Diseases.Biology · 2021Review
- Friend and foe: β-cell CaMolecular metabolism · 2019Review
- Regulation of insulin exocytosis by calcium-dependent protein kinase C in beta cells.Cell calcium · 2017Review
- Human beta cell mass and function in diabetes: Recent advances in knowledge and technologies to understand disease pathogenesis.Molecular metabolism · 2017Review
- Membrane Potential and Calcium Dynamics in Beta Cells from Mouse Pancreas Tissue Slices: Theory, Experimentation, and Analysis.Sensors (Basel, Switzerland) · 2015Review
- Insulin secretion from beta cells within intact islets: location matters.Clinical and experimental pharmacology & physiology · 2015Review
- Using pancreas tissue slices for in situ studies of islet of Langerhans and acinar cell biology.Nature protocols · 2014Article
- The secretory deficit in islets from db/db mice is mainly due to a loss of responding beta cells.Diabetologia · 2014Article
- Uncoupling of Cav1.2 from Ca(2+)-induced Ca(2+) release and SK channel regulation in pancreatic β-cells.Molecular endocrinology (Baltimore, Md.) · 2014Article
- Article
- Mouse pancreas tissue slice culture facilitates long-term studies of exocrine and endocrine cell physiology in situ.PloS one · 2013Article
- Modulation of neuronal pentraxin 1 expression in rat pancreatic β-cells submitted to chronic glucotoxic stress.Molecular & cellular proteomics : MCP · 2012Article
- On depolarization-evoked exocytosis as a function of calcium entry: possibilities and pitfalls.Biophysical journal · 2011Article
- Munc18-1 and Munc18-2 proteins modulate beta-cell Ca2+ sensitivity and kinetics of insulin exocytosis differently.The Journal of biological chemistry · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Goto Kakizaki (GK) rat is a widely used animal model to study defective glucose-stimulated insulin release in type-2 diabetes (T2D). As in T2D patients, the expression of several proteins involved in Ca(2+)-dependent exocytosis of insulin-containing large dense-core vesicles is dysregulated in this model. So far, a defect in late steps of insulin secretion could not be demonstrated. To resolve this apparent contradiction, we studied Ca(2+)-secretion coupling of healthy and GK rat beta cells in acute pancreatic tissue slices by assessing exocytosis with high time-resolution membrane capacitance measurements. We found that beta cells of GK rats respond to glucose stimulation with a normal increase in the cytosolic Ca(2+) concentration. During trains of depolarizing pulses, the secretory activity from GK rat beta cells was defective in spite of upregulated cell size and doubled voltage-activated Ca(2+) currents. In GK rat beta cells, evoked Ca(2+) entry was significantly less efficient in triggering release than in nondiabetic controls. This impairment was neither due to a decrease of functional vesicle pool sizes nor due to different kinetics of pool refilling. Strong stimulation with two successive trains of depolarizing pulses led to a prominent activity-dependent facilitation of release in GK rat beta cells, whereas secretion in controls was unaffected. Broad-spectrum inhibition of PKC sensitized Ca(2+)-dependent exocytosis, whereas it prevented the activity-dependent facilitation in GK rat beta cells. We conclude that a decrease in the sensitivity of the GK rat beta-cell to depolarization-evoked Ca(2+) influx is involved in defective glucose-stimulated insulin secretion. Furthermore, we discuss a role for constitutively increased activity of one or more PKC isoenzymes in diabetic rat beta cells.
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.