Fmoc-L-Leucine

Peroxisome proliferator-activated receptor γ (PPARγ) isoforms heterodimerize with retinoic X receptors to modulate gene expression related to adipocyte differentiation, fatty acid uptake and storage, and glucose metabolism.¹ Natural agonists of PPARγ include fatty acids (e.g., linoleic acid and 15-deoxy-Δ^12,14-prostaglandin J₂), while thiazolidinediones (e.g., rosiglitazone and pioglitazone) are potent synthetic agonists.^2,3 Fmoc-L-leucine is a partial agonist of PPARγ.^2,4 It activates PPARγ with a lower potency (K_i = 15 versus 0.035 µM) but a similar maximal efficacy compared to rosiglitazone.⁴ Fmoc-L-leucine improves insulin resistance in normal, diet-induced glucose-intolerant and in diabetic db/db mice, yet has reduced adipogenic activity.⁴ As a result, it is classified as a selective PPARγ modulator (SPPARM), capable of producing insulin-sensitizing effects while minimizing side effects associated with full agonists.²

WARNING This product is not for human or veterinary use.

1. Heikkinen, S., Auwerx, J., and Argmann, C.A. PPARγ in human and mouse physiology. Biochim. Biophys. Acta 1771(8), 999-1013 (2007).

2. Villacorta, L., Schopfer, F.J., Zhang, J., et al. PPARγ and its ligands: Therapeutic implications in cardiovascular disease. Clin. Sci. (Lond.) 116(3), 205-218 (2009).

3. Zieleniak, A., Wójcik, M., and Wozniak, L.A. Structure and physiological functions of the human peroxisome proliferator-activated receptor γ. Arch. Immunol. Ther. Exp. (Warsz.) 56(5), 331-345 (2008).

4. Rocchi, S., Picard, F., Vamecq, J., et al. A unique PPARγ ligand with potent insulin-sensitizing yet weak adipogenic activity. Mol. Cell 8(4), 737-747 (2001).