Background: Obesity develops when dietary energy intake exceeds energy expenditure, and can be associated with metabolic syndrome. Recent studies have shown that dietary phytochemicals can promote energy expenditure by inducing the browning of white adipose tissue (WAT).
Purpose: This study investigated whether cardamonin induces the browning of 3T3-L1 adipocytes through the activation of protein kinase A (PKA).
Methods: Anti-obesity potential of cardamonin was evaluated in 3T3-L1 adipocytes. Adipocyte-specific genes were observed using western blot, qPCR analysis and immunocytochemistry.
Results: Cardamonin treatment inhibited lipid droplet accumulation and reduced the expression of the adipogenic proteins C/EBPα and FABP4, and the lipogenic proteins LPAATθ, lipin 1, DGAT1, SREBP1, and FAS. Cardamonin also induced the expression of the browning marker genes PRDM16, PGC1α, and UCP1 at the mRNA and protein levels, and induced mRNA expression of CD137, a key marker of beige adipocytes. It also increased the expression of the β-oxidation genes CPT1 and PPARα at the mRNA and protein levels. In addition, cardamonin increased PKA phosphorylation and the mRNA and protein expression of the downstream lipolytic enzymes adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL).
Conclusion: Our findings demonstrate novel effects of cardamonin to stimulate adipocyte browning, suppress lipogenesis, and promote lipolysis, implying it may have potential as an anti-obesity agent.
Keywords: 3T3-L1 cells; Browning; Cardamonin; Lipogenesis; Lipolysis.
Copyright © 2019. Published by Elsevier GmbH.