Evidence map›Paper›PMID 8647933›Full record

ArticleThe Journal of clinical investigation1996

Alterations in basal and glucose-stimulated voltage-dependent Ca2+ channel activities in pancreatic beta cells of non-insulin-dependent diabetes mellitus GK rats.

S Kato, H Ishida, Y Tsuura, K Tsuji, M Nishimura, M Horie, T Taminato, S Ikehara, H Odaka, I Ikeda and 2 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.8field-weighted citation impact, top 7% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 69 citations in OpenAlex.

  1. The spontaneous-diabetes rat: a model of noninsulin dependent diabetes mellitus by Yoshio Goto and Masaei Kakizaki (1981).Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2024
    Review
  2. In Vivo CaBiomedicines · 2023
    Article
  3. Review
  4. Review
  5. Enhanced expression of β cell CaProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  6. Review
  7. Article
  8. An optimized protocol for purification of functional islets of Langerhans.Laboratory investigation; a journal of technical methods and pathology · 2017
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Low-voltage-activated ("T-Type") calcium channels in review.Journal of bioenergetics and biomembranes · 2003
    Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 1 country.

S KatoDepartment of Metabolism and Clinical Nutrition, Kyoto University Faculty of Medicine, Kyoto, Japan.
H Ishida
Y Tsuura
K Tsuji
M Nishimura
M Horie
T Taminato
S Ikehara
H Odaka
I Ikeda
Y Okada
Y Seino
National Institute for Physiological Sciences · JPKyoto University · JPTakeda (Japan) · JPHamamatsu University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In genetically occurring non-insulin-dependent diabetes mellitus (NIDDM) model rats (GK rats), the activities of L- and T-type Ca2+ channels in pancreatic beta cells are found to be augmented, by measuring the Ba2+ currents via these channels using whole-cell patch-clamp technique, while the patterns of the current-voltage curves are indistinguishable. The hyper-responsiveness of insulin secretion to nonglucose depolarizing stimuli observed in NIDDM beta cells could be the result, therefore, of increased voltage-dependent Ca2+ channel activity. Perforated patch-clamp recordings reveal that the augmentation of L-type Ca2+ channel activity by glucose is markedly less pronounced in GK beta cells than in control beta cells, while glucose-induced augmentation of T-type Ca2+ channel activity is observed neither in the control nor in the GK beta cells. This lack of glucose-induced augmentation of L-type Ca2+ channel activity in GK beta cells might be causatively related to the selective impairment of glucose-induced insulin secretion in NIDDM beta cells, in conjunction with an insufficient plasma membrane depolarization due to impaired closure of the ATP-sensitive K+ channels caused by the disturbed intracellular glucose metabolism in NIDDM beta cells.

Indexed as

AnimalsCalciumCalcium ChannelsCalcium Channels, L-TypeCells, CulturedDiabetes Mellitus, Type 2GlucoseInsulinInsulin SecretionIslets of LangerhansMaleMembrane PotentialsModels, BiologicalNitrendipinePatch-Clamp TechniquesPotassiumCalciumCalcium ChannelsCalcium Channels, L-TypeGlucoseInsulinNitrendipinePotassium

Identifiers

PMID8647933
PMCPMC507326
OpenAlexW2016685642

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.