Evidence map›Paper›PMID 25651558›Full record

ArticleAmerican journal of physiology. Renal physiology2015

Cross-talk between insulin and IGF-1 receptors in the cortical collecting duct principal cells: implication for ENaC-mediated Na+ reabsorption.

Daria V Ilatovskaya, Vladislav Levchenko, Michael W Brands, Tengis S Pavlov, Alexander Staruschenko

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Effect of Pituitary-Target Gland Axis on RAAS in the Context of COVID-19.International journal of medical sciences · 2025
    Review
  2. Biomolecules · 2023
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Postprandial effects on electrolyte homeostasis in the kidney.American journal of physiology. Renal physiology · 2019
    Review
  8. Article
  9. Article
  10. Review
  11. Physiological hyperinsulinemia caused by acute hyperglycemia minimizes renal sodium loss by direct action on kidneys.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Article
  12. Insights from direct renal insulin infusion: a new hammer for an age-old nail.American journal of physiology. Renal physiology · 2018
    Article
  13. Article
  14. The normal increase in insulin after a meal may be required to prevent postprandial renal sodium and volume losses.American journal of physiology. Regulatory, integrative and comparative physiology · 2017
    Article
  15. Article
  16. New perspective of ClC-Kb/2 Cl- channel physiology in the distal renal tubule.American journal of physiology. Renal physiology · 2016
    Review
  17. Article
  18. Review
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

5 authors at 2 institutions in 1 country.

Daria V IlatovskayaDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin; and.
Vladislav LevchenkoDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin; and.
Michael W BrandsDepartment of Physiology, Georgia Regents University, Augusta, Georgia.
Tengis S PavlovDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin; and.
Alexander StaruschenkoDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin; and staruschenko@mcw.edu.
Medical College of Wisconsin · USGeorgia Regents Medical Center · US

Funding

Mechanisms for Cardiovascular Control Early in DiabetesR01HL056259 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI BRANDS, MICHAEL W. · 2003 to 2016
$4.4M
Mechanisms and relevance of ENaC regulation by EGF and Rac1R01HL108880 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI STARUSCHENKO, ALEXANDER · 2012 to 2016
$1.9M
Regulation of ENaC in salt-sensitive hypertension via inflammation-induced ROS productionR00HL116603 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI PAVLOV, TENGIS S · 2015 to 2017
$716k
Regulation of ENaC in salt-sensitive hypertension via inflammation-induced ROS prK99HL116603 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI PAVLOV, TENGIS S · 2013 to 2014
$180k
NHLBI NIH HHS K99 HL116603NHLBI NIH HHS K99-HL-116603NHLBI NIH HHS R00 HL116603NHLBI NIH HHS R01 HL056259NHLBI NIH HHS R01-HL-056259NHLBI NIH HHS R01 HL108880NHLBI NIH HHS R01-HL-108880
6 · The paper itself

Abstract

Insulin and IGF-1 are recognized as powerful regulators of the epithelial Na+ channel (ENaC) in the aldosterone-sensitive distal nephron. As previously described, these hormones both acutely increase ENaC activity in freshly isolated split open tubules and cultured principal cortical collecting duct cells. The present study was aimed at differentiating the effects of insulin and IGF-1 on Na+ transport in immortalized mpkCCDcl4 cells and defining their interrelations. We have shown that both insulin and IGF-1 applied basolaterally, but not apically, enhanced transepithelial Na+ transport in the mpkCCDcl4 cell line with EC50 values of 8.8 and 14.5 nM, respectively. Insulin treatment evoked phosphorylation of both insulin and IGF-1 receptors, whereas the effects of IGF-1 were more profound on its own receptor rather than the insulin receptor. AG-1024 and PPP, inhibitors of IGF-1 and insulin receptor tyrosine kinase activity, diminished insulin- and IGF-1-stimulated Na+ transport in mpkCCDcl4 cells. The effects of insulin and IGF-1 on ENaC-mediated currents were found to be additive, with insulin likely stimulating both IGF-1 and insulin receptors. We hypothesize that insulin activates IGF-1 receptors in addition to its own receptors, making the effects of these hormones interconnected.

Indexed as

AnimalsBiological TransportCell LineEpithelial Sodium ChannelsInsulinInsulin-Like Growth Factor IKidney Tubules, CollectingMiceNephronsReceptor, IGF Type 1Receptor, InsulinSignal TransductionSodiumEpithelial Sodium ChannelsInsulinInsulin-Like Growth Factor IReceptor, IGF Type 1Receptor, InsulinSodiumcortical collecting ductepithelial Na+ channelinsulininsulin-like growth factor 1kidneyNa+ transporttyrosine kinase

Identifiers

PMID25651558
PMCPMC4385890
OpenAlexW2000247075

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.