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. Author manuscript; available in PMC: 2019 Dec 5.
Published in final edited form as: Int J Obes (Lond). 2019 Jun 4:10.1038/s41366-019-0379-z. doi: 10.1038/s41366-019-0379-z

Fig. 4. Proposed mechanism of the suppressive effects of Crabp1 in adipogenesis and adipocyte hypertrophy.

Fig. 4.

Pharmacological concentrations of RA (high conc.) inhibit adipocyte adipogenesis through β-catenin pathway to dampen CEBPβ activities. On the other hand, physiological concentrations of RA (low conc.) activate ERK1/2 signaling, promoting CEBPβ activities to trigger adipocyte adipogenesis and hypertrophy. Crabp1 binds RA to reduce free RA availability, thereby dampening ERK1/2 activation and leading to decreased adipogenic signaling. Deleting Crabp1 in CKO would increase RA available to tissues, resulting in enhanced ERK1/2 signaling and its downstream adipogenic signaling. This increases animals’ vulnerability to diet-induced obesity. According to this model, Crabp1 protects mice from developing obesity by reducing the adipogenesis and adipocyte hypertrophy.