Vitamin A signaling in Adipocyte Differentiation: From Molecular Mechanisms to Livestock Production

Adipogenesis, the differentiation of fibroblast-like precursor cells into mature adipocytes, is a complex process governed by transcriptional networks and nutrient signaling. Among micronutrients, vitamin A and its active metabolites, all-trans retinoic acid (atRA), have emerged as potent regulators of adipocyte development, linking nutritional status to metabolic and physiological outcomes. atRA is generated from retinol through sequential oxidation by retinol and aldehyde dehydrogenases and exerts transcriptional control primarily via retinoic acid receptors (RARs) and retinoid X receptors (RXRs). It functions in dynamic crosstalk with Wnt/b-catenin and other signaling pathways to influence the expression of key adipogenic transcription factors, including PPARg and C/EBPa. In vitro evidence from 3T3-L1 and other mammalian cell models demonstrates that low concentrations of atRA (0.01 to 100 nM) promote adipogenic commitment and lipid accumulation, whereas higher concentrations (over 1 uM) inhibit differentiation and stimulate apoptosis through mitochondrial pathways. Comparative in vitro studies across livestock species reveal that atRA exerts species-specific effects which suppresses adipogenesis in porcine and bovine cells, while promoting PPARg-mediated transdifferentiation of avian myoblasts into adipocytes. In vivo, atRA modulates adipose tissue development in a developmental stage-dependent manner, enhancing intramuscular fat deposition during fetal and neonatal stages but suppressing white adipose tissue expansion in adults. Collectively, these finding highlight atRA as a critical integrator of micronutrient signaling, gene regulation, and adipose tissue plasticity. Understanding the mechanisms of atRA-mediated adipogenesis provides key insights into the prevention of metabolic disorders and offers practical strategies in improve meat quality and feed efficiency in animal production system.