Evidence map›Paper›PMID 11283230›Full record

ArticleThe Journal of physiology2001

Somatostatin activates two types of inwardly rectifying K+ channels in MIN-6 cells.

P A Smith, L A Sellers, P P Humphrey

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Somatostatin analogues for the treatment of hyperinsulinaemic hypoglycaemia.Therapeutic advances in endocrinology and metabolism · 2020
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. SSTR2 is the functionally dominant somatostatin receptor in human pancreatic β- and α-cells.American journal of physiology. Endocrinology and metabolism · 2012
    Article
  17. The cellular building blocks of breathing.Comprehensive Physiology · 2012
    Review
  18. Article
  19. Ketogenic diet metabolites reduce firing in central neurons by opening K(ATP) channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    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

3 authors at 1 institution in 1 country.

P A SmithGlaxo Institute of Applied Pharmacology, Department of Pharmacology, Tennis Court Road, Cambridge CB2 1QJ, UK. pas59404@glaxowellcome.co.uk
L A Sellers
P P Humphrey
Wellcome Library · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Western blotting revealed the presence of five somatostatin receptor types, sst1, sst2, sst3, sst4 and sst5, in the mouse pancreatic -cell line MIN-6. In MIN-6 cells, glucose-induced electrical activity was potently (pEC50 = 12.7) and irreversibly reduced by somatostatin (SRIF-14); this was associated with hyperpolarization of the membrane potential (pEC50 = 11.2) and a decrease in the input resistance (pEC50 = 12.7). The effects of SRIF-14 were mimicked by 100 nM L-362,855 (a partial agonist at sst5 receptors), but not BIM-23027 or NNC-26,9100 (selective agonists at sst2 and sst4 receptors, respectively). CH-275 at 100 nM (a selective agonist at sst1 receptors) partially inhibited electrical activity but without membrane potential hyperpolarization. One hundred nanomolar SRIF-28 activated an inwardly rectifying K+ current (ISRIF) ISRIF was activated neither by 1 M BIM-23056 nor CYN-154806 (antagonists at sst5 and sst2 receptors, respectively). The activation of ISRIF by 100 nM SRIF-28 was, however, inhibited 93 % by BIM-23056; CYN-154806 had no effect. Both 100 nM glibenclamide and 200 M tolbutamide, blockers of the -cell ATP-sensitive K+ channel (K-ATP), reduced ISRIF by ~44 %, whereas 1 mM Ba2+ abolished ISRIF. In cell-attached patches, 100 nM SRIF-14 activated two types of single-channel currents whose properties were consistent with those of K-ATP and GIRK channels. In conclusion, somatostatin can inhibit glucose-induced electrical activity in MIN-6 cells by the combined activation of K-ATP and GIRK channels. Studies with selective agonists and antagonists are consistent with this effect being mediated by the sst5 receptor.

Indexed as

Potassium Channels, Inwardly RectifyingAnimalsCell LineGlucoseImmunoblottingIslets of LangerhansKineticsMembrane PotentialsMicePatch-Clamp TechniquesPotassium ChannelsProtein IsoformsReceptors, SomatostatinSomatostatinGlucosePotassium ChannelsPotassium Channels, Inwardly RectifyingProtein IsoformsReceptors, SomatostatinSomatostatin

Identifiers

PMID11283230
PMCPMC2278522
OpenAlexW2131853244

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.