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Genetic variants in DBC1, SIRT1, UCP2 and ADRB2 as potential biomarkers for severe obesity and metabolic complications.

Author information

Affiliations

  • 1. Laboratory of Immunopharmacology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil.
      Authors
    • da Fonseca ACP 1, 2
    • Assis ISDS 1, 2
    • Salum KCR 1, 2, 5
    • Palhinha L 1
    • Maya-Monteiro CM 1
    • Bozza PT 1
    (6 authors)
  • 2. Human Genetics Laboratory, Oswaldo Cruz Institute, Oswaldo Cruz Foundation, Rio de Janeiro, Brazil.
      Authors
    • da Fonseca ACP 1, 2
    • Assis ISDS 1, 2
    • Salum KCR 1, 2, 5
    • Abreu GM 2
    • Zembrzuski VM 2
    • Campos Junior M 2
    • Cambraia A 2
    • Cabello PH 2
    (8 authors)
  • 3. Department of Pathology and Laboratory, Rio de Janeiro State University, Rio de Janeiro, Brazil.
      Authors
    • Nogueira-Neto JF 3
    (1 author)
  • 4. Laboratory of Human and Medical Genetics, Institute of Biological Sciences, Federal University of Pará, Belém, Brazil.
      Authors
    • Souza Junior MLF 4
    (1 author)
  • 5. Clementino Fraga Filho University Hospital, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
      Authors
    • Salum KCR 1, 2, 5
    • Carneiro JRI 5
    (2 authors)

ORCIDs linked to this article

Frontiers in Genetics, 22 May 2024, 15:1363417
https://doi.org/10.3389/fgene.2024.1363417 PMID: 38841722 

Abstract 

Introduction

Obesity is a multifactorial disease associated with the development of many comorbidities. This disease is associated with several metabolic alterations; however, it has been shown that some individuals with obesity do not exhibit metabolic syndrome. Adipose tissue neutralizes the detrimental effects of circulating fatty acids, ectopic deposition, and inflammation, among others, through its esterification into neutral lipids that are stored in the adipocyte. However, when the adipocyte is overloaded, i.e., its expansion capacity is exceeded, this protection is lost, resulting in fatty acid toxicity with ectopic fat accumulation in peripheral tissues and inflammation. In this line, this study aimed to investigate whether polymorphisms in genes that control adipose tissue fat storage capacity are potential biomarkers for severe obesity susceptibility and also metabolic complications.

Methods

This study enrolled 305 individuals with severe obesity (cases, BMI≥35 kg/m2) and 196 individuals with normal weight (controls, 18.5≤BMI≤24.9 kg/m2). Demographic, anthropometric, biochemical, and blood pressure variables were collected from the participants. Plasma levels of leptin, resistin, MCP1, and PAI1 were measured by Bio-Plex 200 Multiplexing Analyzer System. Genomic DNA was extracted and variants in DBC1 (rs17060940), SIRT1 (rs7895833 and rs1467568), UCP2 (rs660339), PPARG (rs1801282) and ADRB2 (rs1042713 and rs1042714) genes were genotyped by PCR allelic discrimination using TaqMan® assays.

Results

Our findings indicated that SIRT1 rs7895833 polymorphism was a risk factor for severe obesity development in the overdominant model. SIRT1 rs1467568 and UCP2 rs660339 were associated with anthropometric traits. SIRT1 rs1467568 G allele was related to lower medians of body adipose index and hip circumference, while the UCP2 rs660339 AA genotype was associate with increased body mass index. Additionally, DBC1 rs17060940 influenced glycated hemoglobin. Regarding metabolic alterations, 27% of individuals with obesity presented balanced metabolic status in our cohort. Furthermore, SIRT1 rs1467568 AG genotype increased 2.5 times the risk of developing metabolic alterations. No statistically significant results were observed with Peroxisome Proliferator-Activated Receptor Gama and ADRB2 polymorphisms.

Discussion/conclusion

This study revealed that SIRT1 rs7895833 and rs1467568 are potential biomarkers for severe obesity susceptibility and the development of unbalanced metabolic status in obesity, respectively. UCP2 rs660339 and DBC1 rs17060940 also showed a significant role in obesity related-traits.

Full text links 

Read article at publisher's site: https://doi.org/10.3389/fgene.2024.1363417

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