Suppression of Fatty Acid and Triglyceride Synthesis by the Flavonoid Orientin through Decrease of C/EBPδ Expression and Inhibition of PI3K/Akt-FOXO1 Signaling in Adipocytes.
Shiori NagaiChihiro MatsumotoMakio ShibanoKo FujimoriPublished in: Nutrients (2018)
Plant flavonoids have a variety of biological properties. In a previous study, we found that the tea of the Asian dayflower, Commelina communis L., decreased the body weight gain in high-fat diet-fed mice. In this study, we studied the anti-adipogenic ability of a flavonoid orientin that is found in abundance in C. communis. Orientin repressed the accumulation of intracellular triglyceride (TG) in mouse adipocyte 3T3-L1 cells. The treatment with orientin also decreased the mRNA levels of the genes involved in adipogenesis, lipogenesis, lipolysis, and TG synthesis, and reduced the release of glycerol. Orientin lowered the expression of CCAAT/enhancer binding protein (C/EBP) δ in the early stage of adipogenesis, leading to a decrease in the expression of the adipogenic master transcription factors such as peroxisome proliferator-activated receptor (PPAR) γ and C/EBPα. Moreover, the anti-adipogenic effect of orientin repressed the phosphorylation of Akt and subsequent phosphorylation of forkhead box protein O1 (FOXO1), which inhibits the transcription of the Ppar gene. These results indicate that a plant flavonoid orientin suppressed the expression of the Pparγ gene through repression of C/ebpδ expression and inhibition of the phosphoinositide 3-kinase /Akt-FOXO1 signaling in adipocytes.
Keyphrases
- binding protein
- transcription factor
- poor prognosis
- pi k akt
- signaling pathway
- adipose tissue
- high fat diet
- insulin resistance
- fatty acid
- high fat diet induced
- early stage
- weight gain
- cell proliferation
- cell cycle arrest
- induced apoptosis
- long non coding rna
- metabolic syndrome
- genome wide
- copy number
- protein kinase
- genome wide identification
- lymph node
- dna methylation
- oxidative stress
- dna binding
- small molecule
- antibiotic resistance genes
- replacement therapy