Transdifferentiation of Myoblasts Into Adipocytes by All-Trans-Retinoic Acid in Avian

Increased adipogenesis in muscle tissues is related to metabolic syndromes and muscle weakness in humans and improvement of meat quality in animal production. With growing evidence for pro-adipogenic functions of all-trans-retinoic acid (atRA), the current study investigated whether atRA can transdifferentiate myoblasts into adipocytes using a quail myogenic cell line (QM7) and avian primary myoblasts. atRA increased cytoplasmic lipid droplet accumulation and mRNA expression for adipogenic genes in these cells. An acute induction of Ppar gamma expression by atRA under cycloheximide treatment indicated a direct regulation of Ppar gamma by atRA. In addition, the induction of Ppar gamma expression was mediated by retinoic acid receptors . At high levels of Ppar gamma by atRA, BADGE, an antagonist of Ppar gamma, inhibited, and rosiglitazone, an agonist of Ppar gamma, further enhanced atRA-induced transdifferentiation. However, at very low levels of Ppar gamma in the absence of atRA treatment, rosiglitazone could not induce transdifferentiation of avian myoblasts. These data suggest that the induction of Ppar gamma expression by atRA is an essential molecular event in myoblasts for atRA-induced transdifferentiation into adipocytes. Based on our findings, atRA can be a new transdifferentiation factor of myoblasts to adipocytes, providing a potential nutrient to enhance marbling in poultry.

Automated summary

This study found that all-trans-retinoic acid (atRA) can induce the transdifferentiation of myoblasts into adipocytes by increasing the expression of Ppar gamma. This discovery provides a new nutrient for enhancing marbling in poultry.