# Functional Foods as Modulators of Epigenetic Mechanisms Affecting Metabolic Health in Adolescence

## TL;DR

This review explores how functional foods can influence epigenetic processes during adolescence to improve metabolic health and prevent diseases like obesity and diabetes.

## Contribution

The paper synthesizes recent evidence on how diet-derived bioactives modulate epigenetic mechanisms affecting metabolic health in adolescents.

## Key findings

- Dietary bioactives influence DNA methylation, histone modifications, and microRNA networks in metabolic pathways.
- Short-chain fatty acids from gut microbiota act as histone deacetylase inhibitors, affecting epigenetic remodeling in adipose tissue.
- Polyphenols and omega-3 fatty acids show potential in counteracting metabolic risks through epigenetic modulation.

## Abstract

Adolescence represents a critical window of metabolic plasticity, during which profound hormonal, neurobiological, and physiological remodelling increases susceptibility to nutritional exposures. In parallel with the rising prevalence of obesity, insulin resistance, metabolic syndrome, and non-alcoholic fatty liver disease among young people, there is growing interest in the potential for functional food components to modulate epigenetic pathways that govern metabolic programming. This narrative review synthesises current evidence (2015–2025) from PubMed, Scopus, Web of Science, and Embase to elucidate how diet-derived bioactive compounds influence epigenetic regulation relevant to adipogenesis, appetite control, insulin signalling, and lipid homeostasis during adolescence. Particular emphasis is placed on molecular mechanisms, including DNA methylation changes in genes regulating adipocyte differentiation, hypothalamic neuropeptide expression, and pancreatic β-cell function; histone modifications, such as acetylation and methylation events that remodel chromatin accessibility in metabolic tissues; and modulation of microRNA networks implicated in lipid metabolism, inflammatory signalling, and insulin secretion. Furthermore, the review examines the interplay between diet, the gut microbiota, and the epigenome, highlighting the role of microbially derived short-chain fatty acids (SCFAs) as endogenous histone deacetylase inhibitors and mediators of epigenetic remodelling in adipose tissue. By linking these mechanisms to specific functional food components, including polyphenols, long-chain omega-3 fatty acids, fermentable dietary fibre, and other bioactive molecules, we demonstrate how nutritional signals can counteract maladaptive metabolic trajectories and potentially reduce the intergenerational transmission of metabolic risk. A deeper understanding of these epigenetic effects provides the foundation for developing personalised nutrition strategies aimed at preventing metabolic disorders from emerging during adolescence and beyond.