Evidence map›Paper›PMID 35112705›Full record

ArticleDisease models & mechanisms2022

An enriched environment re-establishes metabolic homeostasis by reducing obesity-induced inflammation.

Sol Díaz de León-Guerrero, Jonathan Salazar-León, Karla F Meza-Sosa, David Valle-Garcia, Diana Aguilar-León, Gustavo Pedraza-Alva, Leonor Pérez-Martínez

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

  1. Trial
  2. Strategies for optimization of hypoglycemia rat models.Animal models and experimental medicine · 2025
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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

7 authors at 2 institutions in 1 country.

Sol Díaz de León-GuerreroLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), Cuernavaca, Morelos, CP 62210, Mexico.
Jonathan Salazar-LeónLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), Cuernavaca, Morelos, CP 62210, Mexico.
Karla F Meza-SosaLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), Cuernavaca, Morelos, CP 62210, Mexico.
David Valle-GarciaLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), Cuernavaca, Morelos, CP 62210, Mexico.
Diana Aguilar-LeónDepartamento de Patología, Instituto Nacional de Ciencias Médicas y Nutrición 'Salvador Zubirán', Tlalpan, Ciudad de México, CP 14000, Mexico.ORCID 0000-0001-9667-0022
Gustavo Pedraza-AlvaLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), Cuernavaca, Morelos, CP 62210, Mexico.
Leonor Pérez-MartínezLaboratorio de Neuroinmunobiología, Departamento de Medicina Molecular y Bioprocesos, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), Cuernavaca, Morelos, CP 62210, Mexico.ORCID 0000-0003-4163-1653
Universidad Nacional Autónoma de México · MXInstituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity can lead to chronic inflammation in different tissues, generating insulin and leptin resistance and alterations in glucose and lipid metabolism, favoring the development of degenerative diseases, including type II diabetes. Congruently, the inflammatory signaling inhibition prevents the development of obesity and restores insulin sensitivity. Via the enhancement of central nervous system activity, an enriched environment (EE) has beneficial effects on learning and memory as well as on immune cell functions and inflammation in different disease models. Here, we explored whether an EE can restore energy balance in obese mice that previously presented metabolic alterations. We discovered that an EE improved glucose metabolism, increased insulin signaling in liver, and reduced hepatic steatosis and inflammation, and increased lipolysis and browning in the white adipose tissue of high-fat diet (HFD)-fed mice. Finally, we found reduced inflammatory signaling and increased anorexigenic signaling in the hypothalamus of HFD-fed mice exposed to an EE. These data indicate that an EE is able to restore the metabolic imbalance caused by HFD feeding. Thus, we propose EE as a novel therapeutic approach for treating obesity-related metabolic alterations. This article has an associated First Person interview with the first author of the paper.

Indexed as

Diabetes Mellitus, Type 2Insulin ResistanceInsulinsAdipose TissueAnimalsDiet, High-FatHomeostasisHumansInflammationLiverMiceMice, Inbred C57BLObesityInsulinsEnriched environmentInflammationMetabolismObesity

Identifiers

PMID35112705
PMCPMC9227715
OpenAlexW4210778133

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.