An industrialized diet as a determinant of methylation in the 1F region of the NR3C1 gene promoter

Front Nutr. 2024 Apr 3:11:1168715. doi: 10.3389/fnut.2024.1168715. eCollection 2024.

Abstract

Background: Dietary composition can modify gene expression, favoring the development of chronic diseases via epigenetic mechanisms.

Objective: Our study aimed to investigate the relationship between dietary patterns and NR3C1 gene methylation in users of the Brazilian Public Unified Health System (SUS).

Methods: We recruited 250 adult volunteers and evaluated their socioeconomic status, psychosocial characteristics, lifestyle, and anthropometrics. Peripheral blood was collected and evaluated for cortisol levels, glycemia, lipid profile, and insulin resistance; methylation of CpGs 40-47 of the 1F region of the NR3C1 gene was also measured. Factors associated with degree of methylation were evaluated using generalized linear models (p < 0.05). Lifestyle variables and health variables were included as confounding factors.

Results: The findings of our cross-sectional study indicated an association between NR3C1 DNA methylation and intake of processed foods. We also observed relevant associations of average NR3C1 DNA across the segment analyzed, methylation in component 1 (40-43), and methylation in component 2 (44-47) with a pattern of consumption of industrialized products in relation to BMI, serum cortisol levels, and lipid profile. These results may indicate a relationship between methylation and metabolic changes related to the stress response.

Conclusion: These findings suggest an association of methylation and metabolic alterations with stress response. In addition, the present study highlights the significant role of diet quality as a stress-inducing factor that influences NR3C1 methylation. This relationship is further linked to changes in psychosocial factors, lifestyle choices, and cardiometabolic variables, including glucose levels, insulin resistance, and hyperlipidemia.

Keywords: NR3C1 DNA methylation; chronic diseases; diet’s composition; epigenetic mechanisms; food consumption; industrialized diet; lifestyle; metabolic stress.

Grants and funding

This study received support from the Fundação de Amparo à Pesquisa e Inovação do Estado do Espírito Santo - FAPES through the Research Programs of the Unified Health System - PPSUS (PPSUS 10/2013- 65883616/2014 and PPSUS 05/2015 - 59874713515/2016) and FAPES/CNPq - PDCTR (11/2019- 557/2020). We are grateful for the financial support provided by these organizations.