Evidence map›Paper›PMID 26467524›Full record

ArticleJournal of translational medicine2015

Altered liver expression of genes involved in lipid and glucose metabolism in mice with partial IGF-1 deficiency: an experimental approach to metabolic syndrome.

J Rodríguez De Ita, I Castilla-Cortázar, G A Aguirre, C Sánchez-Yago, M Olleros Santos-Ruiz, L Guerra-Menéndez, I Martín-Estal, M García-Magariño, V J Lara-Díaz, J E Puche and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

22 citing papers in PubMed, 41 citations in OpenAlex.

  1. Trial
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  6. Frontiers in cardiovascular medicine · 2022
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  11. Associations betweenAnimals : an open access journal from MDPI · 2020
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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

11 authors at 4 institutions in 2 countries.

J Rodríguez De ItaEscuela de Medicina, Tecnologico de Monterrey, Avenida Morones Prieto No. 3000 Pte. Col. Los Doctores, 64710, Monterrey, Nuevo León, México. julyrdzd@gmail.com.
I Castilla-CortázarEscuela de Medicina, Tecnologico de Monterrey, Avenida Morones Prieto No. 3000 Pte. Col. Los Doctores, 64710, Monterrey, Nuevo León, México. iccortazar@itesm.mx.
G A AguirreEscuela de Medicina, Tecnologico de Monterrey, Avenida Morones Prieto No. 3000 Pte. Col. Los Doctores, 64710, Monterrey, Nuevo León, México. g.amador@itesm.mx.
C Sánchez-YagoDepartment of Medical Physiology, Institute of Applied Molecular Medicine (IMMA), School of Medicine, University CEU San Pablo, Calle Boadilla del Monte s/n, km 5,3, 28668, Madrid, Spain. carmen@rsfarma.es.
M Olleros Santos-RuizFundación de Investigación HM Hospitales, Plaza. del Conde del Valle de Súchil 16, 28015, Madrid, Spain. molleros@fundacionhm.com.
L Guerra-MenéndezDepartment of Medical Physiology, Institute of Applied Molecular Medicine (IMMA), School of Medicine, University CEU San Pablo, Calle Boadilla del Monte s/n, km 5,3, 28668, Madrid, Spain. lguerra@ceu.es.
I Martín-EstalEscuela de Medicina, Tecnologico de Monterrey, Avenida Morones Prieto No. 3000 Pte. Col. Los Doctores, 64710, Monterrey, Nuevo León, México. i.mdelestal@itesm.mx.
M García-MagariñoEscuela de Medicina, Tecnologico de Monterrey, Avenida Morones Prieto No. 3000 Pte. Col. Los Doctores, 64710, Monterrey, Nuevo León, México. magalon@itesm.mx.
V J Lara-DíazEscuela de Medicina, Tecnologico de Monterrey, Avenida Morones Prieto No. 3000 Pte. Col. Los Doctores, 64710, Monterrey, Nuevo León, México. lara-diaz.vj@itesm.mx.
J E PucheDepartment of Medical Physiology, Institute of Applied Molecular Medicine (IMMA), School of Medicine, University CEU San Pablo, Calle Boadilla del Monte s/n, km 5,3, 28668, Madrid, Spain. puche@ceu.es.
U MuñozDepartment of Medical Physiology, Institute of Applied Molecular Medicine (IMMA), School of Medicine, University CEU San Pablo, Calle Boadilla del Monte s/n, km 5,3, 28668, Madrid, Spain. ursula.munozmoron@ceu.es.
Tecnológico de Monterrey · MXUniversidad San Pablo CEU · ESFundación Marques de Valdecilla · ESHM Hospitales · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInsulin growth factor 1 (IGF-1) has multiple effects on metabolism. Much evidence suggests that the deficiency of this hormone increases insulin resistance, impairs lipid metabolism, augments oxidative damage and deregulates the neuro-hormonal axis. An inverse relationship between IGF-1 levels and the prevalence of Metabolic Syndrome (MetS) with its cardiovascular complications has been identified. However, the underlying mechanisms linking IGF-1 and MetS are still poorly understood. In order to elucidate such mechanisms, the aim of this work was to study, in mice with partial IGF-1 deficiency, liver expression of genes involved in glucose and lipid metabolism as well as serum levels of glucose, triglycerides and cholesterol, as well as liver malondialdehyde (MDA) levels, as a marker for oxidative damage.

methodsThree experimental groups were studied in parallel: Controls (CO), wild type mice (igf-1 (+/+)); untreated heterozygous mice (Hz, igf-1 (+/-)) and Hz (igf-1 (+/-)) mice treated with low doses of IGF-1 for 10 days (Hz + IGF-1).

resultsA reduction of IGF-1 serum levels in the Hz group was found, which was normalized by IGF-1 therapy. Serum levels of glucose, triglycerides and cholesterol were significantly increased in the untreated Hz group as compared to both controls and Hz + IGF-1 groups. The expression of genes involved in gluconeogenesis, glycogenolysis, lipid synthesis and transport, and catabolism were altered in untreated Hz animals and the expression of most of them was normalized by IGF-1 therapy; MDA was also significantly increased in the Hz untreated group.

conclusionsThe mere partial IGF-1 deficiency is responsible for the reduction in the expression of genes involved in glucose and lipid metabolism, resulting in dyslipidemia and hyperglycemia. Such genetic alterations may seriously contribute to the establishment of MetS.

Indexed as

Disease Models, AnimalAnimalsBody WeightCarbohydrate MetabolismFatty AcidsGlucoseInsulin-Like Growth Factor Binding ProteinsInsulin-Like Growth Factor ILipid MetabolismLiverMaleMetabolic SyndromeMiceMice, KnockoutOrgan SizeTriglyceridesFatty AcidsGlucoseInsulin-Like Growth Factor Binding ProteinsInsulin-Like Growth Factor ITriglycerides

Identifiers

PMID26467524
PMCPMC4604722
OpenAlexW2101959969

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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.