Chrysin induces brown fat-like phenotype and enhances lipid metabolism in 3T3-L1 adipocytes.

OBJECTIVES: Many studies have to do with promising therapeutic phytochemicals such as flavonoids to treat obesity and related complications, and a number of dietary compounds have been proposed as tools for increasing energy expenditure and decreasing fat accumulation in mammals. Here, we show that the flavonoid chrysin induces browning of 3T3-L1 adipocytes via enhanced expression of brown fat-specific genes and proteins as well as enhances lipid metabolism.
METHODS: Chrysin-induced fat browning was investigated by determining expression levels of brown fat-specific genes and proteins by real-time polymerase chain reaction and immunoblot analysis, respectively.
RESULTS: Chrysin enhanced expression of brown fat-specific markers and increased protein levels of peroxisome proliferator-activated receptor (PPAR)α, PPARγ, PPARδ, phosphorylated AMP-activated protein kinase (p-AMPK), phosphorylated acetyl-CoA carboxylase, hormone sensitive lipase, perilipin, carnitine palmitoyltransferase 1, acyl-coenzyme A oxidase 1, peroxisome proliferator-activated receptor-1 alpha (PGC-1α), and uncoupling protein 1 (UCP-1), suggesting its possible role in augmentation of lipolysis, fat oxidation, and thermogenesis as well as reduction of lipogenesis. Increased expression of UCP-1 and other brown fat-specific markers was possibly mediated by chrysin-induced activation of AMPK based on the fact that inhibition of AMPK by dorsomorphin abolished expression of PR domain-containing 16, UCP-1, and PGC-1α while the activator 5-aminoimidazole-4-carboxamide ribonucleotide elevated expression of these brown marker proteins.
CONCLUSION: Our findings suggest that chrysin plays a dual modulatory role in the form of inducing the brown-like phenotype as well as enhancing lipid metabolism and thus may be explored as a potentially promising food additive for prevention of obesity.