Albizia julibrissin Exerts Anti-Obesity Effects by Inducing the Browning of 3T3L1 White Adipocytes.
Yuna KimHyanggi JiDehun RyuEunae ChoDeokhoon ParkEunsun JungPublished in: International journal of molecular sciences (2023)
This study investigated the effects of the Albizia julibrissin Leaf extracts (AJLE) on adipocytes using 3T3-L1 cells. AJLE inhibited adipogenesis by reducing the expression of peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer binding proteins (C/EBPs) that regulate enzymes involved in fat synthesis and storage, and subsequently reduced intracellular lipid droplets, glycerol-3-phosphate dehydrogenase (GPDH), and triglyceride (TG). AJLE also increased the expression of brown adipocyte markers, such as uncoupling protein-1 (UCP-1), PR/SET domain 16 (PRDM16), and bone morphogenetic protein 7 (BMP7) by inducing the differentiation of brown adipocytes, as shown by a decrease in the lipid droplet sizes and increasing mitochondrial mass. AJLE increased the expression of transcription factor A, mitochondrial (TFAM), mitochondrial DNA (mtDNA) copy number, and UCP-1 protein expression, all of which are key factors in regulating mitochondrial biogenesis. AJLE-induced browning was shown to be regulated by the coordination of AMPK, p38, and SIRT1 signaling pathways. The ability of AJLE to inhibit adipogenesis and induce brown adipocyte differentiation may help treat obesity and related diseases.
Keyphrases
- high fat diet induced
- mitochondrial dna
- copy number
- insulin resistance
- adipose tissue
- poor prognosis
- oxidative stress
- binding protein
- fatty acid
- transcription factor
- metabolic syndrome
- skeletal muscle
- genome wide
- type diabetes
- induced apoptosis
- dna methylation
- signaling pathway
- mesenchymal stem cells
- weight loss
- diabetic rats
- high throughput
- drug induced
- single cell
- gene expression
- long non coding rna
- ischemia reperfusion injury
- reactive oxygen species
- cell cycle arrest
- endoplasmic reticulum stress