Mitochondrial Prx5 overexpression suppresses insulin-induced adipogenesis by downregulating the phosphorylation of p38.
Hye Jin ShinSung Woo LeeMi Hye KimYoung-Ho ParkHong Jun LeeDong-Seok LeePublished in: Bioscience, biotechnology, and biochemistry (2023)
Obesity is caused by the accumulation of excess lipids caused by an energy imbalance. Differentiation of pre-adipocytes induces abnormal lipid accumulation, and reactive oxygen species (ROS) generated in this process promote the differentiation of pre-adipocytes through mitogen-activated protein kinase (MAPK) signaling. Peroxiredoxin (Prx) is a potent antioxidant enzyme, and peroxiredoxin 5 (Prx5), which is mainly expressed in cytosol and mitochondria, inhibits adipogenesis by regulating ROS levels. Based on previous findings, the present study was performed to investigate whether cytosolic Prx5 (CytPrx5) or mitochondrial Prx5 (MtPrx5) has a greater effect on the inhibition of adipogenesis. In this study, MtPrx5 decreased insulin-mediated ROS levels to reduce adipogenic gene expression and lipid accumulation more effectively than CytPrx5. In addition, we found that p38 MAPK mainly participates in adipogenesis. Furthermore, we verified that MtPrx5 overexpression suppressed the phosphorylation of p38 during adipogenesis. Thus, we suggest that MtPrx5 inhibits insulin-induced adipogenesis more effectively than CytPrx5.
Keyphrases
- high fat diet induced
- reactive oxygen species
- type diabetes
- oxidative stress
- gene expression
- cell death
- insulin resistance
- diabetic rats
- dna damage
- metabolic syndrome
- adipose tissue
- glycemic control
- high glucose
- cell proliferation
- skeletal muscle
- protein kinase
- anti inflammatory
- transcription factor
- tyrosine kinase
- physical activity