Catalyzes the saturation of all-trans-retinol to all-trans-13,14-dihydroretinol (PubMed:15358783, PubMed:17253779, PubMed:19139408). Does not exhibit any activity toward all-trans-retinoic acid, nor 9-cis, 11-cis or 13-cis-retinol isomers (PubMed:15358783). May play a role in the metabolism of vitamin A (PubMed:15358783, PubMed:17253779). Independently of retinol conversion, may regulate liver metabolism upstream of MLXIPL/ChREBP (PubMed:28855500). Required for adipocyte differentiation in a 3T3-L1 cell culture model (PubMed:19139408). This effect seems not to mimic the in vivo situation in which animals show increased adiposity in the absence of RETSAT (PubMed:19940255). A + all-trans-13,14-dihydroretinol = AH2 + all-trans-retinol Predominantly expressed in the liver (at protein level) (PubMed:19940255). Also expressed at high levels in kidney, intestine, and white fat and brown fat (PubMed:15358783, PubMed:18289917, PubMed:19139408, PubMed:28855500). Weakly expressed in heart, skeletal muscle and testis and barely detected in the lung, brain and spleen (PubMed:15358783, PubMed:18289917, PubMed:28855500). Up-regulated in the liver of diet-induced obese mice, compared to lean animals (PubMed:28855500). Down-regulated in adipose tissue of obese mice; this decrease could be due to the impact of inflammatory cells on adipocytes (PubMed:19139408). Up-regulated during adipocyte differentiation in a 3T3-L1 cell culture model (at protein level). Up-regulated during starvation (PubMed:18289917). Up-regulated by PPARG (PubMed:19139408). Knockout mice fed either low-fat or high-fat (HFD) diets gain weight at a similar rate as their wild-type littermates and show normal insulin resistance and glucose tolerance. However, they exhibit increased adiposity and increased expression of key adipogenic markers, including PPAR-gamma and its target adipocyte P2 (aP2/FABP4), while maintained on an HFD. Belongs to the carotenoid/retinoid oxidoreductase family. CrtISO subfamily. Truncated N-terminus.