Related Experiment Video
Updated: Jun 18, 2026
08:34
Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
Increased adiposity in the retinol saturase-knockout mouse
Alexander R Moise1, Glenn P Lobo, Bernadette Erokwu
1Department of Pharmacology, University of Kansas, Lawrence, KS, USA. alexmoise@ku.edu
Summary
Retinol saturase (RetSat) deficiency leads to increased body fat accumulation in mice by altering retinoid metabolism. This suggests dihydroretinoids regulate lipid storage and PPARgamma activity.
Area of Science:
- Biochemistry
- Metabolic Research
- Molecular Biology
Background:
- Retinol saturase (RetSat) catalyzes all-trans-retinol to (R)-all-trans-13,14-dihydroretinol.
- RetSat is a peroxisome proliferator-activated receptor (PPAR) gamma target, implicated in adipocyte differentiation.
- The precise role of RetSat in retinoid metabolism and adipogenesis requires further investigation.
Purpose of the Study:
- To elucidate the mechanism behind RetSat's putative proadipogenic effect.
- To investigate the consequences of ablating RetSat expression on retinoid metabolism and adipose tissue differentiation in vivo.
- To understand the impact of RetSat deficiency on lipid accumulation and related molecular pathways.
Main Methods:
- Generation and analysis of RetSat-null mice.
- Assessment of retinoid levels (retinol, retinyl palmitate, dihydroretinol) in liver, serum, and adipose tissue.
- Evaluation of body weight, food intake, and adiposity in RetSat-null and wild-type mice on different diets.
- Analysis of PPARgamma and FABP4/aP2 expression levels.
Main Results:
- RetSat-null mice are deficient in producing all-trans-13,14-dihydroretinol from dietary vitamin A.
- Despite normal retinol and retinyl palmitate levels, RetSat-null mice exhibit increased adiposity.
- Increased adiposity in RetSat-null mice correlates with up-regulation of PPARgamma and its target FABP4/aP2.
- RetSat-null mice maintain similar food intake and weight gain rates compared to wild-type controls.
Conclusions:
- Dihydroretinoids produced by RetSat play a crucial role in regulating lipid accumulation.
- RetSat influences PPARgamma activity, a key regulator of adipogenesis.
- RetSat deficiency leads to increased adiposity through modulation of retinoid metabolism and PPARgamma signaling.
