Retsat reduces atROL to at-13,14-dhROL

Stable Identifier
Mus musculus

All-trans-retinol 13,14-reductase (Retsat) is an ER membrane-associated protein that mediates the saturation of the 13-14 double bond of all-trans-retinol (atROL) to produce all-trans-13,14-dihydroretinol (at-13,14-dhROL) (Moise et al. 2004). The product formed is a metabolite of unknown biological function. Mouse Retsat is expressed in many tissues, with the highest levels in liver, kidney and intestine. In human and mouse, RETSAT is induced during adipogenesis and is directly regulated by the transcription factor peroxisome proliferator activated receptor gamma (PPAR-gamma). Ablation of RETSAT inhibits adipogenesis but this block was not overcome by the product of RETSAT enzymatic activity. In adipose tissue, RETSAT is expressed in adipocytes but is downregulated in obesity. RETSAT could be a novel target for therapeutic intervention in metabolic disease (Schupp et al. 2009).

Literature References
PubMed ID Title Journal Year
19139408 Retinol saturase promotes adipogenesis and is downregulated in obesity Proc. Natl. Acad. Sci. U.S.A. 2009
15358783 Identification of all-trans-retinol:all-trans-13,14-dihydroretinol saturase J. Biol. Chem. 2004
Catalyst Activity
Catalyst Activity
all-trans-retinol 13,14-reductase activity of Retsat [endoplasmic reticulum membrane]
Physical Entity
Orthologous Events