Evidence map›Paper›PMID 28975585›Full record

ArticleMolecular diagnosis & therapy2018

Polymorphisms in Genes Involved in the Leptin-Melanocortin Pathway are Associated with Obesity-Related Cardiometabolic Alterations in a Southern Chilean Population.

Victor Manriquez, Jorge Aviles, Luis Salazar, Nicolas Saavedra, Pamela Seron, Fernando Lanas, Cristina Moreno Fajardo, Mario Hiroyuki Hirata, Rosario Dominguez Crespo Hirata, Alvaro Cerda

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Article in Molecular diagnosis & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

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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

12 citing papers in PubMed, 26 citations in OpenAlex.

  1. Diabetes, metabolic syndrome and obesity : targets and therapy · 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

10 authors at 2 institutions in 2 countries.

Victor ManriquezDepartment of Basic Sciences, Center of Excellence in Translational Medicine, BIOREN, Universidad de La Frontera, Av Alemania 0458, Edificio de Biociencias 4º piso, Temuco, Chile.
Jorge AvilesDepartment of Basic Sciences, Center of Excellence in Translational Medicine, BIOREN, Universidad de La Frontera, Av Alemania 0458, Edificio de Biociencias 4º piso, Temuco, Chile.
Luis SalazarDepartment of Basic Sciences, Center of Molecular Biology and Pharmacogenetics, BIOREN, Universidad de La Frontera, Temuco, Chile.
Nicolas SaavedraDepartment of Basic Sciences, Center of Molecular Biology and Pharmacogenetics, BIOREN, Universidad de La Frontera, Temuco, Chile.
Pamela SeronDepartment of Internal Medicine, Universidad de La Frontera, Temuco, Chile.
Fernando LanasDepartment of Basic Sciences, Center of Molecular Biology and Pharmacogenetics, BIOREN, Universidad de La Frontera, Temuco, Chile.
Cristina Moreno FajardoDepartment of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
Mario Hiroyuki HirataDepartment of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
Rosario Dominguez Crespo HirataDepartment of Clinical and Toxicological Analyses, School of Pharmaceutical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
Alvaro CerdaDepartment of Basic Sciences, Center of Excellence in Translational Medicine, BIOREN, Universidad de La Frontera, Av Alemania 0458, Edificio de Biociencias 4º piso, Temuco, Chile. alvaro.cerda@ufrontera.cl.
Universidad de La Frontera · CLUniversidade de São Paulo · BR

Funding

CNPq-Brazil 462778/2014-2DIUFRO DI15-0017FONDECYT 11150445
6 · The paper itself

Abstract

backgroundPolymorphisms in genes encoding proteins of the leptin-melanocortin pathway have been associated with obesity. The involvement of these polymorphisms with changes in body mass index (BMI) and anthropometric measures could also imply a contribution to the risk of metabolic syndrome (MetS) and metabolic alterations. We evaluated the relationship of leptin-melanocortin system polymorphisms with obesity, MetS, and other metabolic alterations in Southern Chilean individuals.

methodsTwo-hundred individuals were grouped as normoweight (BMI 18.0-24.9 kg/m

resultsLEPR rs1137101 GG genotype was related to reduced risk of obesity (odds ratio [OR] 0.26, 95% confidence interval [CI] 0.08-0.79; p = 0.018) and MetS (OR 0.36, 95% CI 0.15-0.88; p = 0.024), but it was not significant after Bonferroni correction for multiple tests as compared to the AA genotype (p > 0.01). Moreover, LEPR rs1137101 allele G (AG + GG) was related to lower BMI and WHR (p < 0.01). Further multiple linear regression analysis demonstrated that this genotype was also responsible for reduced BMI in 2.44 kg/m

conclusionsThese results suggest that polymorphisms at LEP, LEPR, and MC4R may be useful biomarkers of obesity-related cardiometabolic alterations in our population.

Indexed as

Polymorphism, Single NucleotideAdultCase-Control StudiesChileFemaleGenetic Association StudiesHumansLeptinMaleMetabolic SyndromeMiddle AgedObesityReceptor, Melanocortin, Type 3Receptor, Melanocortin, Type 4Receptors, LeptinLEP protein, humanLEPR protein, humanLeptinMC3R protein, humanMC4R protein, humanReceptor, Melanocortin, Type 3Receptor, Melanocortin, Type 4Receptors, Leptin

Identifiers

PMID28975585
OpenAlexW2760854947

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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.