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Lentinan depresses 3T3-L1 fat cell formation by inhibiting PPARγ/AKT signaling pathway
1Department of Pediatric Surgery, The Second Hospital of Shandong University, Jinan, China.
Abstract:
We investigated the mechanism of the effect of lentinan on 3T3-L1 fat cell formation by inhibiting the peroxisome proliferator-activated receptor gamma (PPARγ)/protein kinase B (AKT) signaling pathway. 3T3-L1 fat cells were treated with 80 mM lentinan with or without the PPARγ activator, 100 mM rosiglitazone for 24 h. Reverse transcription-polymerase chain reaction was applied to detect PPARγ and AKT mRNA expression levels. Western blotting was used to detect AKT protein expression level. Compared with the control group, 80 mM lentinan increased PPARγ mRNA expression and downregulated AKT mRNA expression. After treatment with rosiglitazone, PPARγ mRNA expression increased by 78% (P < 0.05), while AKT mRNA expression decreased by 71% (P < 0.05). Lentinan treatment decreased AKT protein expression by 33%, and AKT protein expression in the lentinan and rosiglitazone co-treatment group was reduced by 28% compared with the lentinan treatment group. We found that 80 mM lentinan increased PPARγ mRNA expression and reduced AKT mRNA. Combination treatment with rosiglitazone increased this effect. This suggests that lentinan can depress 3T3-L1 fat cell formation by inhibiting the PPARγ/AKT signaling pathway.
Insights
Lentinan inhibits fat cell formation by downregulating the peroxisome proliferator-activated receptor gamma (PPARγ)/protein kinase B (AKT) pathway. This study reveals lentinan
Area of Science:
- Biochemistry
- Cell Biology
- Molecular Biology
Background:
- Adipogenesis, or fat cell formation, is regulated by complex signaling pathways.
- The peroxisome proliferator-activated receptor gamma (PPARγ)/protein kinase B (AKT) pathway plays a crucial role in adipogenesis.
- Understanding the molecular mechanisms underlying adipogenesis is vital for metabolic disease research.
Purpose of the Study:
- To investigate the mechanism by which lentinan affects 3T3-L1 fat cell differentiation.
- To determine the role of the PPARγ/AKT signaling pathway in lentinan-mediated inhibition of adipogenesis.
Main Methods:
- 3T3-L1 fibroblasts were treated with lentinan and/or rosiglitazone (a PPARγ activator).
- Reverse transcription-polymerase chain reaction (RT-PCR) was used to quantify mRNA expression of PPARγ and AKT.
- Western blotting was employed to assess AKT protein levels.
Main Results:
- Lentinan treatment significantly increased PPARγ mRNA expression and decreased AKT mRNA expression in 3T3-L1 cells.
- Co-treatment with rosiglitazone further enhanced PPARγ mRNA upregulation and AKT mRNA downregulation.
- Lentinan treatment led to a significant decrease in AKT protein expression, an effect potentiated by rosiglitazone.
Conclusions:
- Lentinan inhibits 3T3-L1 fat cell formation by modulating the PPARγ/AKT signaling pathway.
- The findings suggest lentinan's potential as a therapeutic agent for conditions associated with excessive adipogenesis.
- Lentinan's mechanism involves the upregulation of PPARγ and downregulation of AKT signaling.
