Evidence map›Paper›PMID 31918912›Full record

ArticleMolecular metabolism2020

Specific knockout of p85α in brown adipose tissue induces resistance to high-fat diet-induced obesity and its metabolic complications in male mice.

Almudena Gomez-Hernandez, Andrea R Lopez-Pastor, Carlota Rubio-Longas, Patrik Majewski, Nuria Beneit, Vanesa Viana-Huete, Gema García-Gómez, Silvia Fernandez, Marta Letizia Hribal, Giorgio Sesti and 2 more

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 22% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. New Mediators in the Crosstalk between Different Adipose Tissues.International journal of molecular sciences · 2024
    Pooled it
  2. Article
  3. Article
  4. The Role of PIK3R1 in Metabolic Function and Insulin Sensitivity.International journal of molecular sciences · 2023
    Review
  5. Review
  6. Review
  7. Article
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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

12 authors at 3 institutions in 2 countries.

Almudena Gomez-HernandezBiochemistry and Molecular Biology Department, School of Pharmacy, Complutense University of Madrid, Spain; Health Research Institute of San Carlos Clinic Hospital (IdISSC), Madrid, Spain; CIBER of Diabetes and Associated Metabolic Diseases (CIBERDEM), Spain. Electronic address: algomezh@ucm.es.
Andrea R Lopez-PastorBiochemistry and Molecular Biology Department, School of Pharmacy, Complutense University of Madrid, Spain; Health Research Institute of San Carlos Clinic Hospital (IdISSC), Madrid, Spain. Electronic address: andreara@ucm.es.
Carlota Rubio-LongasBiochemistry and Molecular Biology Department, School of Pharmacy, Complutense University of Madrid, Spain. Electronic address: carrub05@ucm.es.
Patrik MajewskiBiochemistry and Molecular Biology Department, School of Pharmacy, Complutense University of Madrid, Spain. Electronic address: patmajewski94@gmail.com.
Nuria BeneitBiochemistry and Molecular Biology Department, School of Pharmacy, Complutense University of Madrid, Spain; Health Research Institute of San Carlos Clinic Hospital (IdISSC), Madrid, Spain. Electronic address: nubere87@hotmail.com.
Vanesa Viana-HueteBiochemistry and Molecular Biology Department, School of Pharmacy, Complutense University of Madrid, Spain; Health Research Institute of San Carlos Clinic Hospital (IdISSC), Madrid, Spain. Electronic address: vanesa.viana.h@gmail.com.
Gema García-GómezHealth Research Institute of San Carlos Clinic Hospital (IdISSC), Madrid, Spain; CIBER of Diabetes and Associated Metabolic Diseases (CIBERDEM), Spain. Electronic address: ggarciag@ucm.es.
Silvia FernandezHealth Research Institute of San Carlos Clinic Hospital (IdISSC), Madrid, Spain; CIBER of Diabetes and Associated Metabolic Diseases (CIBERDEM), Spain. Electronic address: silferna@ucm.es.
Marta Letizia HribalDepartment of Medical and Surgical Sciences, University Magna Graecia of Catanzaro, Italy. Electronic address: hribal@unicz.it.
Giorgio SestiDepartment of Medical and Surgical Sciences, University Magna Graecia of Catanzaro, Italy. Electronic address: sesti@unicz.it.
Oscar EscribanoBiochemistry and Molecular Biology Department, School of Pharmacy, Complutense University of Madrid, Spain; Health Research Institute of San Carlos Clinic Hospital (IdISSC), Madrid, Spain; CIBER of Diabetes and Associated Metabolic Diseases (CIBERDEM), Spain. Electronic address: oescriba@ucm.es.
Manuel BenitoBiochemistry and Molecular Biology Department, School of Pharmacy, Complutense University of Madrid, Spain; Health Research Institute of San Carlos Clinic Hospital (IdISSC), Madrid, Spain; CIBER of Diabetes and Associated Metabolic Diseases (CIBERDEM), Spain. Electronic address: mbenito@ucm.es.
Universidad Complutense de Madrid · ESCentro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas · ESMagna Graecia University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveAn increase in mass and/or brown adipose tissue (BAT) functionality leads to an increase in energy expenditure, which may be beneficial for the prevention and treatment of obesity. Moreover, distinct class I PI3K isoforms can participate in metabolic control as well as in systemic dysfunctions associated with obesity. In this regard, we analyzed in vivo whether the lack of p85α in BAT (BATp85αKO) could modulate the activity and insulin signaling of this tissue, thereby improving diet-induced obesity and its associated metabolic complications.

methodsWe generated BATp85αKO mice using Cre-LoxP technology, specifically deleting p85α in a conditional manner. To characterize this new mouse model, we used mice of 6 and 12 months of age. In addition, BATp85αKO mice were submitted to a high-fat diet (HFD) to challenge BAT functionality.

resultsOur results suggest that the loss of p85α in BAT improves its thermogenic functionality, high-fat diet-induced adiposity and body weight, insulin resistance, and liver steatosis. The potential mechanisms involved in the improvement of obesity include (1) increased insulin signaling and lower activation of JNK in BAT, (2) enhanced insulin receptor isoform B (IRB) expression and association with IRS-1 in BAT, (3) lower production of proinflammatory cytokines by the adipose organ, (4) increased iWAT browning, and (5) improved liver steatosis.

conclusionsOur results provide new mechanisms involved in the resistance to obesity development, supporting the hypothesis that the gain of BAT activity induced by the lack of p85α has a direct impact on the prevention of diet-induced obesity and its associated metabolic complications.

Indexed as

Adipose Tissue, BrownAnimalsClass Ia Phosphatidylinositol 3-KinaseDiet, High-FatMaleMiceMice, Inbred C57BLMice, KnockoutObesityClass Ia Phosphatidylinositol 3-KinaseBrown adipose tissueInsulin resistanceObesityp85αWhite adipose tissue

Identifiers

PMID31918912
PMCPMC6977168
OpenAlexW2988942022

What OpenQuestion 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 OpenQuestion graph.