Evidence map›Paper›PMID 21140140›Full record

ArticleThe Journal of membrane biology2011

Glucose-induced regulation of NHEs activity and SGLTs expression involves the PKA signaling pathway.

Olívia Beloto-Silva, Ubiratan Fabres Machado, Maria Oliveira-Souza

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in The Journal of membrane biology, 2011. 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
0.8field-weighted citation impact, top 28% 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, 48 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Histamine regulates the activity and the expression of the NaInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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  8. Sweet Taste Signaling: The Core Pathways and Regulatory Mechanisms.International journal of molecular sciences · 2022
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  13. A role for tubular NaAmerican journal of physiology. Renal physiology · 2020
    Article
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  16. Review
  17. SGLT inhibitors attenuate NO-dependent vascular relaxation in the pulmonary artery but not in the coronary artery.American journal of physiology. Lung cellular and molecular physiology · 2015
    Article
  18. Probing SGLT2 as a therapeutic target for diabetes: basic physiology and consequences.Diabetes & vascular disease research · 2015 · on this map
    Review
  19. Angiotensin receptor blocker telmisartan suppresses renal gluconeogenesis during starvation.Diabetes, metabolic syndrome and obesity : targets and therapy · 2015
    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.

Olívia Beloto-SilvaDepartment of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, São Paulo, SP 05508-900, Brazil.
Ubiratan Fabres Machado
Maria Oliveira-Souza
Universidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The effect of glucose on the intracellular pH (pH(i)) recovery rate (dpH(i)/dt) and Na(+)-glucose transporter (SGLT) localization was investigated in HEK-293 cells, a cell line that expresses endogenous NHE1, NHE3, SGLT1, and SGLT2 proteins. The activity of the Na(+)/H(+) exchangers (NHEs) was evaluated by using fluorescence microscopy. The total and membrane protein expression levels were analyzed by immunoblotting. In cells cultivated in 5 mM glucose, the pH(i) recovery rate was 0.169 ± 0.020 (n = 6). This value did not change in response to the acute presence of glucose at 2 or 10 mM, but decreased with 25 mM glucose, an effect that was not observed with 25 mM mannitol. Conversely, the chronic effect of high glucose (25 mM) increased the pH(i) recovery rate (~40%, P < 0.05), without changes in the total levels of NHE1, NHE3, or SGLT1 expression, but increasing the total cellular (~50%, P < 0.05) and the plasma membrane (~100%, P < 0.01) content of SGLT2. Treatment with H-89 (10(-6) M) prevented the stimulatory effect of chronic glucose treatment on the pH(i) recovery rate and SGLT2 expression in the plasma membrane. Our results indicate that the effect of chronic treatment with a high glucose concentration is associated with increased NHEs activity and plasma membrane expression of SGLT2 in a protein kinase A-dependent way. The present results reveal mechanisms of glucotoxicity and may contribute to understanding the diabetes-induced damage of this renal epithelial cell.

Indexed as

BiotinylationCation Transport ProteinsCell LineCyclic AMP-Dependent Protein KinasesGlucoseHumansImmunoblottingSignal TransductionSodium-Glucose Transporter 1Sodium-Glucose Transporter 2Sodium-Hydrogen Exchanger 1Sodium-Hydrogen Exchanger 3Sodium-Hydrogen ExchangersCation Transport ProteinsCyclic AMP-Dependent Protein KinasesGlucoseSLC5A1 protein, humanSLC5A2 protein, humanSLC9A1 protein, humanSLC9A3 protein, humanSodium-Glucose Transporter 1Sodium-Glucose Transporter 2Sodium-Hydrogen Exchanger 1Sodium-Hydrogen Exchanger 3Sodium-Hydrogen Exchangers

Identifiers

PMID21140140
OpenAlexW2093606464

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.