Evidence map›Paper›PMID 24976401›Full record

ArticleBiochemical and biophysical research communications2014

NHE1 deficiency in liver: implications for non-alcoholic fatty liver disease.

Vikram Prasad, Shivani Chirra, Rohit Kohli, Gary E Shull

Abstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

11 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Dynamic NaeLife · 2021
    Article
  8. Review
  9. Pathophysiology of hepatic NaExperimental and therapeutic medicine · 2020
    Review
  10. NBCe1 NaWorld journal of cardiology · 2018
    Article
  11. 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

4 authors at 1 institution in 1 country.

Vikram PrasadDepartment of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati College of Medicine, United States. Electronic address: prasadvm@ucmail.uc.edu.
Shivani ChirraDepartment of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati College of Medicine, United States.
Rohit KohliDepartment of Gastroenterology, Hepatology, and Nutrition, Cincinnati Children's Hospital, University of Cincinnati, Cincinnati, OH 45267, United States.
Gary E ShullDepartment of Molecular Genetics, Biochemistry, and Microbiology, University of Cincinnati College of Medicine, United States.
University of Cincinnati Medical Center · US

Funding

MODELS FOR GENETIC DISORDERS OF ACID-BASE TRANSPORTR37DK050594 · NIDDK · UNIVERSITY OF CINCINNATI · PI SHULL, GARY EDWARD · 2000 to 2009
$6.0M
MODELS FOR GENETIC DISORDERS OF ACID BASE TRANSPORTR01DK050594 · NIDDK · UNIVERSITY OF CINCINNATI · PI SHULL, GARY EDWARD · 1996 to 2013
$1.9M
NIDDK NIH HHS DK050594NIDDK NIH HHS R01 DK050594NIDDK NIH HHS R37 DK050594
6 · The paper itself

Abstract

Non-alcoholic fatty liver disease NAFLD is closely associated with the dysregulation of lipid homeostasis. Diet-induced hepatic steatosis, which can initiate NAFLD progression, has been shown to be dramatically reduced in mice lacking the electroneutral Na(+)/H(+) exchanger NHE1 (Slc9a1). In this study, we investigated if NHE1 deficiency had effects in liver that could contribute to the apparent protection against aberrant lipid accumulation. RT-PCR and immunoblot analyses of wild-type and NHE1-null livers revealed an expression profile that strongly suggested attenuation of both de novo lipogenesis and hepatic stellate cell activation, which is implicated in liver fibrosis. This included upregulation of the farnesoid X receptor FXR, peroxisome proliferator-activated receptor PPARγ, its co-activator PGC1α, and sestrin 2, an antioxidant protein involved in hepatic metabolic homeostasis. Furthermore, expression levels of the pro-lipogenic liver X receptor LXRα, and acetyl CoA carboxylases 1 and 2 were downregulated. These changes were associated with evidence of reduced cellular stress, which persisted even upon exposure to a high-fat diet, and the better preservation of insulin signaling, as evidenced by protein kinase B/Akt phosphorylation (Ser473). These results indicate that NHE1 deficiency may protect against NAFLD pathogenesis, which is significant given the availability of highly specific NHE1 inhibitors.

Indexed as

AnimalsBiomarkersCation Transport ProteinsDietary FatsEndoplasmic Reticulum StressFatty LiverInsulinLipid MetabolismLiverMice, KnockoutNon-alcoholic Fatty Liver DiseaseOxidative StressSignal TransductionSodium-Hydrogen Exchanger 1Sodium-Hydrogen ExchangersBiomarkersCation Transport ProteinsDietary FatsInsulinSlc9a1 protein, mouseSodium-Hydrogen Exchanger 1Sodium-Hydrogen ExchangersInsulin resistanceLiver fibrosisMetabolic syndromeNHE1ObesitySteatohepatitis

Identifiers

PMID24976401
PMCPMC4111981
OpenAlexW1984685441

What OpenQuestion holds

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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.