Evidence map›Paper›PMID 32546857›Full record

ArticleInternational journal of obesity (2005)2021

Weight loss normalizes enhanced expression of the oncogene survivin in visceral adipose tissue and blood leukocytes from individuals with obesity.

Andrea G Izquierdo, Marcos C Carreira, Gemma Rodriguez-Carnero, Alfredo Fernandez-Quintela, Aurelio M Sueiro, Miguel A Martinez-Olmos, German Guzman, Daniel De Luis, Marcela A S Pinhel, Carolina F Nicoletti and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in International journal of obesity (2005), 2021. 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
1.0field-weighted citation impact, top 23% 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, 11 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

16 authors at 7 institutions in 2 countries.

Andrea G Izquierdo *Epigenomics in Endocrinology and Nutrition Group, Instituto de Investigacion Sanitaria (IDIS), Complejo Hospitalario Universitario de Santiago (CHUS/SERGAS), Santiago de Compostela, Spain.ORCID http://orcid.org/0000-0002-0846-8834
Marcos C Carreira *CIBER Fisiopatologia de la Obesidad y Nutricion (CIBERobn), Madrid, Spain.
Gemma Rodriguez-CarneroEpigenomics in Endocrinology and Nutrition Group, Instituto de Investigacion Sanitaria (IDIS), Complejo Hospitalario Universitario de Santiago (CHUS/SERGAS), Santiago de Compostela, Spain.
Alfredo Fernandez-QuintelaCIBER Fisiopatologia de la Obesidad y Nutricion (CIBERobn), Madrid, Spain.
Aurelio M SueiroMolecular Endocrinology Group, Instituto de Investigacion Sanitaria (IDIS), Complejo Hospitalario Universitario de Santiago (CHUS/SERGAS) and Santiago de Compostela University (USC), Santiago de Compostela, Spain.
Miguel A Martinez-OlmosEpigenomics in Endocrinology and Nutrition Group, Instituto de Investigacion Sanitaria (IDIS), Complejo Hospitalario Universitario de Santiago (CHUS/SERGAS), Santiago de Compostela, Spain.
German GuzmanMedical Department Pronokal, Pronokal Group, Barcelona, Spain.
Daniel De LuisEndocrinology and Nutrition Research Center, School of Medicine, Department of Endocrinology and Nutrition, Hospital Clinico Universitario, University of Valladolid, Valladolid, Spain.ORCID http://orcid.org/0000-0002-1745-9315
Marcela A S PinhelDepartment of Internal Medicine, Laboratory of Nutrigenomic Studies, Ribeirao Preto Medical School, FMRP, University of Sao Paulo, USP, Sao Paulo, Brazil.
Carolina F NicolettiDepartment of Internal Medicine, Laboratory of Nutrigenomic Studies, Ribeirao Preto Medical School, FMRP, University of Sao Paulo, USP, Sao Paulo, Brazil.
Carla B NoninoDepartment of Internal Medicine, Laboratory of Nutrigenomic Studies, Ribeirao Preto Medical School, FMRP, University of Sao Paulo, USP, Sao Paulo, Brazil.
Francisco J OrtegaCIBER Fisiopatologia de la Obesidad y Nutricion (CIBERobn), Madrid, Spain.ORCID http://orcid.org/0000-0003-0039-1593
Maria P PortilloCIBER Fisiopatologia de la Obesidad y Nutricion (CIBERobn), Madrid, Spain.
Jose M Fernandez-RealCIBER Fisiopatologia de la Obesidad y Nutricion (CIBERobn), Madrid, Spain.
Felipe F CasanuevaCIBER Fisiopatologia de la Obesidad y Nutricion (CIBERobn), Madrid, Spain.
Ana B CrujeirasEpigenomics in Endocrinology and Nutrition Group, Instituto de Investigacion Sanitaria (IDIS), Complejo Hospitalario Universitario de Santiago (CHUS/SERGAS), Santiago de Compostela, Spain. anabelencrujeiras@hotmail.com.ORCID http://orcid.org/0000-0003-4392-0301
Complejo Hospitalario Universitario de Santiago · ESUniversidade de São Paulo · BRInstitut d'Investigació Biomèdica de Girona · ESUniversity of the Basque Country · ESInstituto de Salud Carlos III · ESPronoKal Group (Spain) · ESUniversidad de Valladolid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectivesSurvivin is an oncogene associated with a decrease in apoptosis, an increase in tumor growth, and poor clinical outcome of diverse malignancies. A correlation between obesity, cancer, and survivin is reported in the literature. To date, the impact of weight loss on change in survivin levels is understudied. This study was aimed at: (1) comparing survivin levels in adipose tissue (AT) from lean and obese animal models and evaluating changes after weight loss induced by energy restriction and/or exercise; (2) comparing survivin levels in normal weighted and obese humans and evaluating changes in survivin levels after weight loss induced by a very-low-calorie ketogenic diet (VLCKD) or bariatric surgery in AT and/or blood leukocytes (PBL/PBMCs). SUBJECTS/

methodsSurvivin expression was evaluated in subcutaneous (SAT) and visceral (VAT) AT derived from animal models of monogenic (Zucker rats) and diet-induced obesity (Sprague Dawley rats and C57BL/6J mice) and after a 4-week weight-loss protocol of energy restriction and/or exercise. Plasma was used to measure the inflammatory status. Survivin expression was also evaluated in PBMCs from patients with obesity and compared with normal weight, in PBLs after VLCKD, and in SAT and/or PBLs after bariatric surgery.

resultsSurvivin expression was specifically higher in VAT from obese that lean animals, without differences in SAT. It decreased after weight loss induced by energy restriction and correlated with adiposity and inflammatory markers. In humans, the correlation between being obese and higher levels of survivin was confirmed. In obese subjects, survivin levels were reduced following weight loss after either VLCKD or bariatric surgery. Particularly, a decrease in PBMCs expression (not in SAT one) was found after surgery.

conclusionsWeight loss is effective in decreasing survivin levels. Also, PBL/PBMC should be regarded as appropriate mirror of survivin levels in VAT for the identification of an obesity-related protumoral microenvironment.

Indexed as

SurvivinAdultAnimalsFemaleHumansIntra-Abdominal FatLeukocytes, MononuclearMaleMiceMice, Inbred C57BLMiddle AgedObesityRatsRats, Sprague-DawleyRats, ZuckerWeight LossBIRC5 protein, humanSurvivin

Identifiers

PMID32546857
PMCPMC7752753
OpenAlexW3034851398

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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.