Abstract
Bee venom (BV) has been widely used in the treatment of certain immune-related diseases. It has been used for pain relief and in the treatment of chronic inflammatory diseases. Despite its extensive use, there is little documented evidence to demonstrate its medicinal utility against obesity. In this study, we demonstrated the inhibitory effects of BV on adipocyte differentiation in 3T3-L1 cells and on a high fat diet (HFD)-induced obesity mouse model through the inhibition of adipogenesis. BV inhibited lipid accumulation, visualized by Oil Red O staining, without cytotoxicity in the 3T3-L1 cells. Male C57BL/6 mice were fed either a HFD or a control diet for 8 weeks, and BV (0.1 mg/kg or 1 mg/kg) or saline was injected during the last 4 weeks. BV-treated mice showed a reduced body weight gain. BV was shown to inhibit adipogenesis by downregulating the expression of the transcription factors CCAAT/enhancer-binding proteins (C/EBPs) and the peroxisome proliferator-activated receptor gamma (PPARγ), using RT-qPCR and Western blotting. BV induced the phosphorylation of AMP-activated kinase (AMPK) and acetyl-CoA carboxylase (ACC) in the cell line and in obese mice. These findings demonstrate that BV mediates anti-obesity/differentiation effects by suppressing obesity-related transcription factors.
Highlights
Obesity is defined as an abnormal or excessive fat accumulation that presents a risk to health.Adipocyte hyperplasia and hypertrophy are determinant factors of obesity [1]
Hyperplasia and lipid accumulation are known to occur in the 3T3-L1 cell line during differentiation [8,27]. 3T3-L1 cells were treated with Bee venom (BV)
Adipocyte differentiation and lipid accumulation are both processes related to the development of obesity [35]
Summary
Obesity is defined as an abnormal or excessive fat accumulation that presents a risk to health.Adipocyte hyperplasia and hypertrophy are determinant factors of obesity [1]. 3T3-L1 preadipocytes have been used in studies regarding adipogenesis and differentiation These cells differentiate in response to adipogenic inducers including insulin, dexamethasone, and 3-isobutyl-1-methylxanthine (IBMX) [4]. Confluent cells enter a growth arrest phase [5,6]. These growth-arrested cells subsequently restart the cell cycle and increase cell numbers three- to four-fold during the MCE phase [7]. This hyperplasia during cell differentiation is related to the production of specific adipogenic transcription factors [8]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
