Uncoupling Proteins Variants Are Linked to Hypercholesterolemia and Abdominal Obesity in Metabolically Unhealthy Women.

1 · What the graph read from it

What it found

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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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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

Beyond the Scale: How Metabolic Context Reveals Hidden Genetic Risks.Lifestyle genomics · 2026
Article

4 · The record

Corrections and comments

Erratum issued
Erratum.2025

5 · Who and what money

Authors and funding

5 authors.

Erika Sierra-RuelasDoctorado en Ciencias de la Nutrición Traslacional, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Jalisco, Mexico.

Nathaly Torres-CastilloDoctorado en Ciencias de la Nutrición Traslacional, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Jalisco, Mexico.

Barbara VizmanosDoctorado en Ciencias de la Nutrición Traslacional, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Jalisco, Mexico.

Wendy Campos PérezDoctorado en Ciencias de la Nutrición Traslacional, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Jalisco, Mexico.

Erika Martínez-LópezDoctorado en Ciencias de la Nutrición Traslacional, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Jalisco, Mexico.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionIt has been reported that even with the same body mass index (BMI); there are subjects with metabolically healthy (MH) or unhealthy (MUH) phenotype. The main determinants of the unhealthy phenotype are the type and distribution of fat, ectopic fat accumulation, genetics, and lifestyle factors. Uncoupling proteins (UCPs) disengage mitochondrial respiration from ATP synthesis and result in heat production, which in turn is related to energy expenditure and, thus, to fat mass accumulation. The association of the UCP1 3826A/G (rs1800592), UCP2 Ala55Val (rs660339), and UCP3 55C/T (rs1800849) variants with metabolic variables was evaluated according to metabolic phenotype in Mexican women.

methodsWomen aged 18-65 years classified as normal weight (NW) or excessive weight (EW) according to their BMI (from 18.5 to <25 kg/m2 for NW, and from 25 to <40 kg/m2 for EW), were included. Participants were classified into two metabolic phenotypes: MH or MUH, respectively, based on ATP-III criteria and the homeostasis model assessment of insulin resistance (HOMA-IR). The genetic variants were determined by allelic discrimination using TaqMan® probes.

resultsIn participants with the UCP1 3826A/G variant, an increased risk of hypercholesterolemia was observed in those with the NW-MUH phenotype (OR = 5.09, 95% CI = 1.03-25.12, p = 0.017). The UCP2 Ala55Val variant in EW-MUH subjects was associated with higher abdominal obesity risk (OR = 3.23, 95% CI = 1.21-8.60, p = 0.019), while no associations were found with the UCP3 55C/T variant.

conclusionUCP1 and UCP2 variants are related with hypercholesterolemia and visceral fat accumulation in women with MUH phenotype.

introductionIt has been reported that even with the same body mass index (BMI); there are subjects with metabolically healthy (MH) or unhealthy (MUH) phenotype. The main determinants of the unhealthy phenotype are the type and distribution of fat, ectopic fat accumulation, genetics, and lifestyle factors. Uncoupling proteins (UCPs) disengage mitochondrial respiration from ATP synthesis and result in heat production, which in turn is related to energy expenditure and, thus, to fat mass accumulation. The association of the UCP1 3826A/G (rs1800592), UCP2 Ala55Val (rs660339), and UCP3 55C/T (rs1800849) variants with metabolic variables was evaluated according to metabolic phenotype in Mexican women.

methodsWomen aged 18-65 years classified as normal weight (NW) or excessive weight (EW) according to their BMI (from 18.5 to <25 kg/m2 for NW, and from 25 to <40 kg/m2 for EW), were included. Participants were classified into two metabolic phenotypes: MH or MUH, respectively, based on ATP-III criteria and the homeostasis model assessment of insulin resistance (HOMA-IR). The genetic variants were determined by allelic discrimination using TaqMan® probes.

resultsIn participants with the UCP1 3826A/G variant, an increased risk of hypercholesterolemia was observed in those with the NW-MUH phenotype (OR = 5.09, 95% CI = 1.03-25.12, p = 0.017). The UCP2 Ala55Val variant in EW-MUH subjects was associated with higher abdominal obesity risk (OR = 3.23, 95% CI = 1.21-8.60, p = 0.019), while no associations were found with the UCP3 55C/T variant.

conclusionUCP1 and UCP2 variants are related with hypercholesterolemia and visceral fat accumulation in women with MUH phenotype.

Indexed as

HypercholesterolemiaMitochondrial Uncoupling ProteinsObesity, AbdominalUncoupling Protein 1Uncoupling Protein 2AdolescentAdultAgedBody Mass IndexEnergy MetabolismFemaleGenetic Predisposition to DiseaseHumansInsulin ResistanceMexicoMiddle AgedMitochondrial Uncoupling ProteinsUCP1 protein, humanUCP2 protein, humanUCP3 protein, humanUncoupling Protein 1Uncoupling Protein 2Uncoupling Protein 3CholesterolMetabolic disturbancesUncoupling proteinWaist circumference