Evidence map›Paper›PMID 25085841›Full record

ReviewExperimental physiology2014

Intestinal regulation of urinary sodium excretion and the pathophysiology of diabetic kidney disease: a focus on glucagon-like peptide 1 and dipeptidyl peptidase 4.

Volker Vallon, Neil G Docherty

Open access · bronzeAbstract readReview
In one paragraph

Review in Experimental physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Role of obesity in chronic kidney disease progression.Current research in physiology · 2025
    Review
  4. Glomerular pressure and tubular oxygen supply: a critical dual target for renal protection.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Review
  5. Review
  6. Article
  7. Renoprotective Effects of DPP-4 Inhibitors.Antioxidants (Basel, Switzerland) · 2021
    Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. 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
  13. Article
  14. Review
  15. Article
  16. Review
  17. 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

2 authors at 2 institutions in 2 countries.

Volker VallonDepartment of Medicine, University of California San Diego, La Jolla, CA, USA Department of Pharmacology, University of California San Diego, La Jolla, CA, USA Department of Veterans Affairs, San Diego Healthcare System, San Diego, CA, USA vvallon@ucsd.edu.
Neil G DochertyDiabetes Complications Research Centre, Conway Institute of Biomolecular and Biomedical Research, School of Medicine and Medical Sciences, University College Dublin, Belfield, Dublin 4, Ireland.
University College Dublin · IEUniversity of California, San Diego · US

Funding

UAB-UCSD O'Brien Core Center for Acute Kidney Injury ResearchP30DK079337 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SANDERS, PAUL W. · 2008 to 2022
$18.3M
GLOMERULAR AND TUBULAR FUNCTION IN THE DIABETIC KIDNEYR01DK056248 · NIDDK · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI THOMSON, SCOTT CULVER · 1999 to 2014
$4.6M
Blood Pressure Regulation by OAT3R01HL094728 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ERALY, SATISH A, VALLON, VOLKER · 2010 to 2014
$1.9M
NHLBI NIH HHS R01 HL094728NIDDK NIH HHS P30 DK079337NIDDK NIH HHS R01 DK056248
6 · The paper itself

Abstract

The tubular hypothesis of glomerular filtration and nephropathy in diabetes is a pathophysiological concept that assigns a critical role to the tubular system, including proximal tubular hyper-reabsorption and growth, which is relevant for early glomerular hyperfiltration and later chronic kidney disease. Here we focus on how harnessing the bioactivity of hormones released from the gut may ameliorate the early effects of diabetes on the kidney in part by attenuating proximal tubular hyper-reabsorption and growth. The endogenous tone of the glucagon-like peptide 1 (GLP-1)/GLP-1 receptor (GLP-1R) system and its pharmacological activation are nephroprotective in diabetes independent of changes in blood glucose. This is associated with suppression of increases in kidney weight and glomerular hyperfiltration, which may reflect, at least in part, its inhibitory effects on tubular hyper-reabsorption and growth. Inhibition of dipeptidyl peptidase 4 (DPP-4) is also nephroprotective independent of changes in blood glucose and involves GLP-1/GLP-1R-dependent and -independent mechanisms. The GLP-1R agonist exendin-4 induces natriuresis via activation of the GLP-1R. In contrast, DPP4 inhibition increases circulating GLP-1, but drives a GLP-1R-independent natriuretic response, implying a role for other DPP-4 substrates. The extent to which the intrarenal DPP-4/GLP-1 receptor system contributes to all these changes remains to be established, as does the direct impact of the system on renal inflammation.

Indexed as

NatriuresisAnimalsBlood GlucoseDiabetic NephropathiesDipeptidyl Peptidase 4Dipeptidyl-Peptidase IV InhibitorsGlomerular Filtration RateGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorHumansIntestinal MucosaIntestinesKidney Tubules, ProximalReceptors, GlucagonRenal EliminationSignal TransductionBlood GlucoseDipeptidyl Peptidase 4Dipeptidyl-Peptidase IV InhibitorsDPP4 protein, humanGLP1R protein, humanGlucagon-Like Peptide 1Glucagon-Like Peptide-1 ReceptorReceptors, GlucagonSodium

Identifiers

PMID25085841
PMCPMC4162767
OpenAlexW1544427581

What OpenQuestion holds

Textmetadata
LicenceTDM
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.