Evidence map›Paper›PMID 30135311›Full record

ArticleJCI insight2018

Renal tubule insulin receptor modestly promotes elevated blood pressure and markedly stimulates glucose reabsorption.

Jonathan M Nizar, Blythe D Shepard, Vianna T Vo, Vivek Bhalla

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
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  19. Effects ofMedicina (Kaunas, Lithuania) · 2019
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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

4 authors at 2 institutions in 1 country.

Jonathan M NizarDivision of Nephrology, Department of Medicine, Stanford University School of Medicine, Stanford, California, USA.
Blythe D ShepardDepartment of Human Science, Georgetown University, Washington, DC.
Vianna T VoDivision of Nephrology, Department of Medicine, Stanford University School of Medicine, Stanford, California, USA.
Vivek BhallaDivision of Nephrology, Department of Medicine, Stanford University School of Medicine, Stanford, California, USA.
Stanford University · USGeorgetown University · US

Funding

Spectrum Stanford Center for clinical and Translational Research and EducationUL1TR001085 · NCATS · STANFORD UNIVERSITY · PI CULLEN, MARK RICHARD, GREENBERG, HARRY BERNARD · 2013 to 2017
$37.1M
ENaC Transport in Insulin Resistance: Role of Insulin & IGF-1 ReceptorsR01DK091565 · NIDDK · STANFORD UNIVERSITY · PI BHALLA, VIVEK · 2011 to 2015
$2.0M
Contribution of Renal Tubule Insulin Receptor on Proximal Tubule Sodium Transport and Hypertension int he Metabolic SyndromeK08DK114567 · NIDDK · UNIVERSITY OF IOWA · PI NIZAR, JONATHAN · 2017 to 2021
$831k
Elucidating the Role of Olfactory Receptor 1393 in Renal Glucose HandlingK01DK106400 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI SHEPARD, BLYTHE D · 2016 to 2021
$657k
NCATS NIH HHS UL1 TR001085NIDDK NIH HHS K01 DK106400NIDDK NIH HHS K08 DK114567NIDDK NIH HHS R01 DK091565
6 · The paper itself

Abstract

Although the cause of hypertension among individuals with obesity and insulin resistance is unknown, increased plasma insulin, acting in the kidney to increase sodium reabsorption, has been proposed as a potential mechanism. Insulin may also stimulate glucose uptake, but the contributions of tubular insulin signaling to sodium or glucose transport in the setting of insulin resistance is unknown. To directly study the role of insulin signaling in the kidney, we generated inducible renal tubule-specific insulin receptor-KO mice and used high-fat feeding and mineralocorticoids to model obesity and insulin resistance. Insulin receptor deletion did not alter blood pressure or sodium excretion in mice on a high-fat diet alone, but it mildly attenuated the increase in blood pressure with mineralocorticoid supplementation. Under these conditions, KO mice developed profound glucosuria. Insulin receptor deletion significantly reduced SGLT2 expression and increased urinary glucose excretion and urine flow. These data demonstrate a direct role for insulin receptor-stimulated sodium and glucose transport and a functional interaction of insulin signaling with mineralocorticoids in vivo. These studies uncover a potential mechanistic link between preserved insulin sensitivity and renal glucose handling in obesity and insulin resistance.

Indexed as

AnimalsBlood PressureDiet, High-FatDisease Models, AnimalFludrocortisoneGlucoseGlycosuriaHumansHypertensionInsulinInsulin ResistanceKidney TubulesMaleMiceMice, KnockoutObesityFludrocortisoneGlucoseInsulinReceptor, InsulinSodium, DietaryDiabetesEndocrinologyHypertensionInsulin signalingNephrology

Identifiers

PMID30135311
PMCPMC6141164
OpenAlexW2888086634

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.