Evidence mapPaperPMID 32916153Full record

ArticleMetabolism: clinical and experimental2020

Hepatic insulin-degrading enzyme regulates glucose and insulin homeostasis in diet-induced obese mice.

Beatriz Merino, Cristina M Fernández-Díaz, Cristina Parrado-Fernández, Carlos M González-Casimiro, Tamara Postigo-Casado, Carmen D Lobatón, Malcolm A Leissring, Irene Cózar-Castellano, Germán Perdomo

Open access · hybridAbstract read
In one paragraph

Article in Metabolism: clinical and experimental, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

27 citing papers in PubMed, 43 citations in OpenAlex.

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  18. Insects as a New Complex Model in Hormonal Basis of Obesity.International journal of molecular sciences · 2021
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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

9 authors at 5 institutions in 3 countries.

Beatriz MerinoInstituto de Biología y Genética Molecular (University of Valladolid-CSIC), Valladolid, Spain.
Cristina M Fernández-DíazInstituto de Biología y Genética Molecular (University of Valladolid-CSIC), Valladolid, Spain. Electronic address: cristinamaria.fernandez@imdea.org.
Cristina Parrado-FernándezInstituto de Biología y Genética Molecular (University of Valladolid-CSIC), Valladolid, Spain; AlzeCure Pharma AB, Huddinge, Sweden.
Carlos M González-CasimiroInstituto de Biología y Genética Molecular (University of Valladolid-CSIC), Valladolid, Spain. Electronic address: carlosmanuel.gonzalez.casimiro@uva.es.
Tamara Postigo-CasadoInstituto de Biología y Genética Molecular (University of Valladolid-CSIC), Valladolid, Spain. Electronic address: tamara.postigo@uva.es.
Carmen D LobatónInstituto de Biología y Genética Molecular (University of Valladolid-CSIC), Valladolid, Spain. Electronic address: clobaton@ibgm.uva.es.
Malcolm A LeissringInstitute for Memory Impairments and Neurological Disorders, University of California, Irvine (UCI MIND), Irvine, CA, USA. Electronic address: m.leissring@uci.edu.
Irene Cózar-CastellanoInstituto de Biología y Genética Molecular (University of Valladolid-CSIC), Valladolid, Spain; Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Madrid, Spain. Electronic address: irene.cozar@uva.es.
Germán PerdomoInstituto de Biología y Genética Molecular (University of Valladolid-CSIC), Valladolid, Spain; Departamento de Ciencias de la Salud, Universidad de Burgos, Burgos, Spain. Electronic address: g.perdomo@csic.es.
Instituto de Biomedicina y Genética Molecular de Valladolid · ESUniversidad de Valladolid · ESAlzeCure Pharma (Sweden) · SECentro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas · ESUniversity of California, Irvine · US

Funding

NIGMS NIH HHS R01 GM115617
6 · The paper itself

Abstract

The insulin-degrading enzyme (IDE) is a metalloendopeptidase with a high affinity for insulin. Human genetic polymorphisms in Ide have been linked to increased risk for T2DM. In mice, hepatic Ide ablation causes glucose intolerance and insulin resistance when mice are fed a regular diet.

objectiveThese studies were undertaken to further investigate its regulatory role in glucose homeostasis and insulin sensitivity in diet-induced obesity.

methodsTo this end, we have compared the metabolic effects of loss versus gain of IDE function in mice fed a high-fat diet (HFD).

resultsWe demonstrate that loss of IDE function in liver (L-IDE-KO mouse) exacerbates hyperinsulinemia and insulin resistance without changes in insulin clearance but in parallel to an increase in pancreatic β-cell function. Insulin resistance was associated with increased FoxO1 activation and a ~2-fold increase of GLUT2 protein levels in the liver of HFD-fed mice in response to an intraperitoneal injection of insulin. Conversely, gain of IDE function (adenoviral delivery) improves glucose tolerance and insulin sensitivity, in parallel to a reciprocal ~2-fold reduction in hepatic GLUT2 protein levels. Furthermore, in response to insulin, IDE co-immunoprecipitates with the insulin receptor in liver lysates of mice with adenoviral-mediated liver overexpression of IDE.

conclusionsWe conclude that IDE regulates hepatic insulin action and whole-body glucose metabolism in diet-induced obesity via insulin receptor levels.

Indexed as

Diet, High-FatHomeostasisAnimalsGlucoseInsulinInsulysinLiverMaleMiceMice, ObeseGlucoseIde protein, mouseInsulinInsulysinDiabetesGlucose transportersHepatic insulin resistanceHigh-fat dietInsulin-degrading enzymeInsulin receptor

Identifiers

PMID32916153
PMCPMC8616598
OpenAlexW3084048874

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.