Abstract
Mastoparan B (MP-B), a cationic tetradecapeptide isolated from the venom of the Vespa basalis, exhibits cardiovascular effects, local edema and antibacterial activity. In this study, the anti-adipogenic effect of an MP-B analogue and its mechanism of action in 3T3-L1 preadipocytes were studied. The MP-B analogue (MP-B12) inhibited preadipocyte differentiation and decreased the expression of adipogenic transcription factors, including CCAAT/enhancer binding protein-alpha (C/EBPα), nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ) and sterol regulatory element-binding protein-1 (SREBP-1). Moreover, MP-B12 regulated the phosphorylation of Akt and glycogen synthase kinase-3 beta (GSK-3β), both of which play a role in preadipocyte differentiation, in which insulin and certain growth factors stimulated adipogenesis. This study demonstrates that MP-B12 inhibits preadipocyte differentiation and the accumulation of lipid droplets in 3T3-L1 preadipocytes and could potentially be used to treat obesity.Video Clip of Methodology:4 min 11 sec Full Screen Alternate
Highlights
Adipose tissue plays a crucial role in the energy storage, lipid homeostasis and fatty acid release
We evaluated the inhibitory effects of Mastoparan B (MP-B) and MP-B12 on adipogenesis, and investigated how MP-B12 acts to reduce the differentiation of preadipocytes into adipocytes
The quantification of the extracted Oil Red O stain showed that the lipid content was strongly reduced by 10 μM MP-B12 compared to positive control (Figure 1)
Summary
Adipose tissue plays a crucial role in the energy storage, lipid homeostasis and fatty acid release. Several drugs have been used to treat obesity, such as orlistat, sibutramine, dinitrophenol, and thyroid hormone These drugs can cause serious adverse effects, including dry mouth, insomnia, anorexia and valvular heart disease (Halford, 2006). 3T3-L1 preadipocytes differentiate upon exposure to inducers, such as insulin, 3-isobutyl-1-methylxanthine and dexamethasone (Kanda et al, 2012) This treatment initiates early events in adipogenesis, which depend on the coordinated regulation of gene expression (Ho et al, 2013; Lee et al, 2013). Adipogenic transcription factors, such as C/EBPα, PPARγ and SREBP-1, are the key regulators of adipogenesis (Kang et al, 2013a). These factors cooperate to promote the expression of adipogenic genes that cause terminal differentiation of
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