Abstract
Phenolic compounds might modulate adiposity. Here, we report our observation that polyphenols and phenolic acids inhibit adipogenesis in 3T3-L1 with different intensity depending on the family and the stage of differentiation. While quercetin and resveratrol inhibited lipid accumulation along the whole process of differentiation, apigenin and myricetin were active during the early and latest stages, but not intermediate, contrary to hesperidin. The activity of phenolic acids was limited to the early stages of the differentiation process, except p-coumaric and ellagic acids. This anti-adipogenic effect was accompanied by down-regulation of Scd1 and Lpl. Molecular docking analysis revealed that the inhibitory activity of these phenolic compounds over the early stages of adipogenesis exhibits a significant correlation (r = 0.7034; p = 0.005) with their binding affinity to the ligand-binding domain of PPARγ. Results show that polyphenols and phenolic acids would interact with specific residues of the receptor, which could determine their potential anti-adipogenic activity during the early stages of the differentiation. Residues Phe264, His266, Ile281, Cys285 and Met348 are the most frequently involved in these interactions, which might suggest a crucial role for these amino acids modulating the activity of the receptor. These data contribute to elucidate the possible mechanisms of phenolic compounds in the control of adipogenesis.
Highlights
At a cellular level, obesity is characterized by the increase in the number and size of adipocytes, which are differentiated from fibroblastic preadipocytes in adipose tissue [1]
One of the most promising mechanisms by which bioactive compounds counteract obesity is the inhibition of adipogenesis, either by blocking the initial preadipocytic differentiation, or by preventing the fat accumulation needed for the adipocyte maturation [29,30]
We evaluated the expression of some additional adipocyte-specific genes that are regulated by peroxisome proliferator-activated receptor γ (PPARγ)
Summary
Obesity is characterized by the increase in the number and size of adipocytes, which are differentiated from fibroblastic preadipocytes in adipose tissue [1]. Based on its important role regulating both adipocyte differentiation and subsequent lipogenesis, the nuclear hormone receptor PPARγ has emerged as an interesting pharmacological target to control adipogenesis [4,5] This receptor contains six domains, the ligand-binding domain (LBD) constitutes the major part of the protein and is responsible for the ability of PPARγ to direct adipogenesis and regulate insulin sensitivity [5]. In this sense, different molecules have emerged as biological ligands of PPARγ, interacting with variable affinity with the LBD and possibly modulating the activity of this receptor. These molecules have been proposed as a promising strategy to manage obesity and related diseases [6,7,8]
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