Evidence map›Paper›PMID 24418844›Full record

ArticleInternational journal of obesity (2005)2014

Reduced hepatic aquaporin-9 and glycerol permeability are related to insulin resistance in non-alcoholic fatty liver disease.

A Rodríguez, P Gena, L Méndez-Giménez, A Rosito, V Valentí, F Rotellar, I Sola, R Moncada, C Silva, M Svelto and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in International journal of obesity (2005), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 6% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.

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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

13 authors at 3 institutions in 2 countries.

A Rodríguez1] Metabolic Research Laboratory, Clínica Universidad de Navarra, Pamplona, Spain [2] CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Pamplona, Spain.
P GenaDepartment of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari Aldo Moro, Bari, Italy.
L Méndez-GiménezMetabolic Research Laboratory, Clínica Universidad de Navarra, Pamplona, Spain.
A RositoDepartment of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari Aldo Moro, Bari, Italy.
V Valentí1] CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Pamplona, Spain [2] Department of Surgery, Clínica Universidad de Navarra, Pamplona, Spain.
F Rotellar1] CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Pamplona, Spain [2] Department of Surgery, Clínica Universidad de Navarra, Pamplona, Spain.
I SolaDepartment of Pathology, Clínica Universidad de Navarra, Pamplona, Spain.
R MoncadaDepartment of Anesthesia, Clínica Universidad de Navarra, Pamplona, Spain.
C SilvaDepartment of Endocrinology and Nutrition, Clínica Universidad de Navarra, Pamplona, Spain.
M Svelto1] Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari Aldo Moro, Bari, Italy [2] Centro di Eccellenza di Genomica in campo Biomedico ed Agrario (CEGBA), Bari, Italy.
J SalvadorDepartment of Endocrinology and Nutrition, Clínica Universidad de Navarra, Pamplona, Spain.
G Calamita1] Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari Aldo Moro, Bari, Italy [2] Centro di Eccellenza di Genomica in campo Biomedico ed Agrario (CEGBA), Bari, Italy.
G Frühbeck1] Metabolic Research Laboratory, Clínica Universidad de Navarra, Pamplona, Spain [2] CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Instituto de Salud Carlos III, Pamplona, Spain [3] Department of Endocrinology and Nutrition, Clínica Universidad de Navarra, Pamplona, Spain.
Clinica Universidad de Navarra · ESUniversity of Bari Aldo Moro · ITInstituto de Salud Carlos III · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectivesGlycerol represents an important metabolite for the control of lipid accumulation and hepatic gluconeogenesis. We investigated whether hepatic expression and functionality of aquaporin-9 (AQP9), a channel mediating glycerol influx into hepatocytes, is impaired in non-alcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH) in the context of insulin resistance. SUBJECTS/

methodsLiver biopsies were obtained from 66 morbid obese patients undergoing bariatric surgery (66% women, mean body mass index (BMI) 46.1±1.0 kg m(-2)) with available liver echography and pathology analysis of the biopsies in this cross-sectional study. Subjects were classified according to normoglycemia (NG), impaired glucose tolerance (IGT) or type 2 diabetes (T2D). Hepatic expression of AQP9 was analyzed by real-time PCR, western blotting and immunohistochemistry, while glycerol permeability (P(gly)) was measured by stopped-flow light scattering.

resultsAQP9 was the most abundantly (P<0.0001) expressed aquaglyceroporin in human liver (AQP9>>>AQP3>AQP7>AQP10). Obese patients with T2D showed increased plasma glycerol as well as lower P(gly) and hepatic AQP9 expression. The prevalence of NAFLD and NASH in T2D patients was 100 and 65%, respectively. Interestingly, AQP9 expression was decreased in patients with NAFLD and NASH as compared with those without hepatosteatosis, in direct relation to the degree of steatosis and lobular inflammation, being further reduced in insulin-resistant individuals. The association of AQP9 with insulin sensitivity was independent of BMI and age. Consistent with these data, fasting insulin and C-reactive protein contributed independently to 33.1% of the hepatic AQP9 mRNA expression variance after controlling for the effects of age and BMI.

conclusionsAQP9 downregulation together with the subsequent reduction in hepatic glycerol permeability in insulin-resistant states emerges as a compensatory mechanism whereby the liver counteracts further triacylglycerol accumulation within its parenchyma as well as reduces hepatic gluconeogenesis in patients with NAFLD.

Indexed as

AdultAquaporinsBlotting, WesternC-Reactive ProteinCross-Sectional StudiesDown-RegulationFatty LiverFemaleGlucose IntoleranceGlycerolHumansInsulin ResistanceLiverMaleNon-alcoholic Fatty Liver DiseasePermeabilityAQP9 protein, humanAquaporinsC-Reactive ProteinGlycerolTriglycerides

Identifiers

PMID24418844
OpenAlexW2052405103

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.