# Vitamin A Derivatives and Adipose Tissue Differentiation: Molecular Pathways Driving Browning and Anti-Obesity Effects

**Authors:** Billur Bilikozen Aygun, Berrak Basturk, Aylin Ayaz

PMC · DOI: 10.1007/s13679-025-00684-2 · 2026-01-15

## TL;DR

This review explores how vitamin A and carotenoids affect fat tissue, promoting browning and reducing obesity through metabolic changes.

## Contribution

The paper highlights new insights into how retinoids and carotenoids regulate fat metabolism and browning, offering potential nutrition-based anti-obesity strategies.

## Key findings

- Retinoids and carotenoids reduce fat formation by suppressing key genes like PPARγ and SREBP1-c.
- These compounds promote browning of white fat via AMPK activation and upregulation of thermogenic genes like UCP1.
- They improve metabolic balance by reducing inflammation and increasing mitochondrial activity in fat tissue.

## Abstract

This review aims to evaluate the effects of retinoids and carotenoids (β-carotene, lycopene, lutein, and β-cryptoxanthin) on adipose tissue biology, particularly browning processes, in light of the current literature. In the current era of increasing global obesity prevalence, understanding the potential regulatory roles of these lipophilic micronutrients in energy homeostasis and adipose tissue plasticity may contribute to the development of new nutrition-based or pharmacological strategies.

The regulatory roles of vitamin A (VA) and carotenoids in adipose tissue metabolism have been intensively investigated in recent years. Current findings indicate that compounds such as retinoic acid, lycopene, β-cryptoxanthin, and zeaxanthin reduce adipogenesis and lipogenesis by suppressing the expression of peroxisome proliferator-activated receptor gamma (PPARγ), CCAAT/enhancer binding protein alpha (C/EBPα), and sterol regulatory element-binding protein 1c (SREBP1-c) while increasing energy expenditure and promoting the browning of white adipose tissue through the activation of 5′-adenosine monophosphate-activated protein kinase (AMPK) and the upregulation of thermogenic genes such as uncoupling protein 1 (UCP1), PR domain containing 16 (PRDM16), and PPARγ coactivator-1α (PGC-1α). These effects are associated with reduced adipocyte hypertrophy, increased mitochondrial activity, and decreased systemic inflammation.

VA and carotenoids exert multifaceted effects on adipose tissue differentiation and energy metabolism, suggesting an alternative pathway against obesity. By reducing lipid storage, stimulating thermogenesis, and enhancing oxidative metabolism, these bioactive compounds help restore metabolic balance. Overall, evidence indicates that VA derivatives and carotenoids, through adipose tissue browning and improved metabolic efficiency, represent promising nutrition-based strategies to combat obesity.

## Linked entities

- **Genes:** PPARG (peroxisome proliferator activated receptor gamma) [NCBI Gene 5468], CEBPA (CCAAT enhancer binding protein alpha) [NCBI Gene 1050], Srebf1 (sterol regulatory element binding transcription factor 1) [NCBI Gene 78968], UCP1 (uncoupling protein 1) [NCBI Gene 7350], PRDM16 (PR/SET domain 16) [NCBI Gene 63976], PPARGC1A (PPARG coactivator 1 alpha) [NCBI Gene 10891]
- **Proteins:** PUMP1 (plant uncoupling mitochondrial protein 1)
- **Chemicals:** retinoic acid (PubChem CID 444795), lycopene (PubChem CID 446925), β-cryptoxanthin (PubChem CID 5281235), zeaxanthin (PubChem CID 5280899), vitamin A (PubChem CID 445354)
- **Diseases:** obesity (MONDO:0011122)

## Full-text entities

- **Diseases:** Obesity (MESH:D009765)
- **Chemicals:** Vitamin A (MESH:D014801)

## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12804335/full.md

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Source: https://tomesphere.com/paper/PMC12804335