Evidence map›Paper›PMID 21106690›Full record

ArticleAmerican journal of physiology. Cell physiology2011

Insulin activates epithelial sodium channel (ENaC) via phosphoinositide 3-kinase in mammalian taste receptor cells.

Arian F Baquero, Timothy A Gilbertson

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 49 citations in OpenAlex.

  1. ENAC blockade reduces blood pressure and arterial stiffness in adults with obesity and insulin resistance.American journal of physiology. Heart and circulatory physiology · 2026
    Trial
  2. Pharmaceutical agents targeting KThe journal of physiological sciences : JPS · 2026
    Article
  3. Article
  4. Endocrinology of Taste with Aging.Endocrinology and metabolism clinics of North America · 2023
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Gastrointestinal-Renal Axis: Role in the Regulation of Blood Pressure.Journal of the American Heart Association · 2017
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  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

2 authors at 1 institution in 1 country.

Arian F BaqueroDepartment of Biology and The Center for Advanced Nutrition, Utah State University, Logan, USA. arian.baquero@ucdenver.edu
Timothy A Gilbertson
Utah State University · US

Funding

NIDCD P30 Core: Rocky Mountain Taste and Smell CenterP30DC004657 · NIDCD · UNIVERSITY OF COLORADO DENVER · PI KINNAMON, SUE C., RESTREPO, DIEGO · 2000 to 2014
$7.6M
Mechanisms of sweet transduction in mammalian taste budsR01DC006021 · NIDCD · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI CHAUDHARI, NIRUPA · 2003 to 2011
$2.8M
Taste Transduction and its RegulationR01DC002507 · NIDCD · UTAH STATE UNIVERSITY · PI GILBERTSON, TIMOTHY A. · 2003 to 2007
$1.2M
SALT TASTE TRANSDUCTION AND ITS HORMONAL REGULATIONR29DC002507 · NIDCD · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI GILBERTSON, TIMOTHY A. · 1995 to 1999
–
NIDCD NIH HHS DC02507NIDCD NIH HHS P30 DC004657NIDCD NIH HHS P30 DC04657NIDCD NIH HHS R01 DC006021
6 · The paper itself

Abstract

Diabetes is a profound disease that results in a severe lack of regulation of systemic salt and water balance. From our earlier work on the endocrine regulation of salt taste at the level of the epithelial sodium channel (ENaC), we have begun to investigate the ability of insulin to alter ENaC function with patch-clamp recording on isolated mouse taste receptor cells (TRCs). In fungiform and vallate TRCs that exhibit functional ENaC currents (e.g., amiloride-sensitive Na(+) influx), insulin (5-20 nM) caused a significant increase in Na(+) influx at -80 mV (EC(50) = 7.53 nM). The insulin-enhanced currents were inhibited by amiloride (30 μM). Similarly, in ratiometric Na(+) imaging using SBFI, insulin treatment (20 nM) enhanced Na(+) movement in TRCs, consistent with its action in electrophysiological assays. The ability of insulin to regulate ENaC function is dependent on the enzyme phosphoinositide 3-kinase since treatment with the inhibitor LY294002 (10 μM) abolished insulin-induced changes in ENaC. To test the role of insulin in the regulation of salt taste, we have characterized behavioral responses to NaCl using a mouse model of acute hyperinsulinemia. Insulin-treated mice show significant avoidance of NaCl at lower concentrations than the control group. Interestingly, these differences between groups were abolished when amiloride (100 μM) was added into NaCl solutions, suggesting that insulin was regulating ENaC. Our results are consistent with a role for insulin in maintaining functional expression of ENaC in mouse TRCs.

Indexed as

AmilorideAnimalsBehavior, AnimalEpithelial Sodium ChannelsInsulinInsulin Receptor Substrate ProteinsMaleMiceMice, Inbred C57BLPatch-Clamp TechniquesPhosphatidylinositol 3-KinasesPhosphatidylinositolsReceptor, InsulinReceptors, G-Protein-CoupledSodiumSodium Channel BlockersAmilorideEpithelial Sodium ChannelsInsulinInsulin Receptor Substrate ProteinsIrs2 protein, mousePhosphatidylinositol 3-KinasesPhosphatidylinositolsReceptor, InsulinReceptors, G-Protein-CoupledSodiumSodium Channel BlockersSodium, Dietary

Identifiers

PMID21106690
PMCPMC3074626
OpenAlexW2159866558

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.