• 대한의용생체공학회:의공학회지
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• 제39권3호
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• pp.109-115
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• 2018

Obesity is a worldwide disease caused by the excessive proliferation of adipocytes. Multiple factors, including melatonin and physical loading, are involved in the control of obesity. Melatonin has been shown to induce apoptosis on preadipocytes while physical loading such as fluid shear stress (FSS) affects the proliferation and differentiation of adipocytes. Here, we studied the combined effects of melatonin and FSS on 3T3-L1 preadipocytes. For physical loading, preadipocytes were stimulated with a maximum dynamic fluid shear stress of 1 Pa at 1 Hz for 2 hours with/without melatonin. The experiment conditions were divided into four groups: (1) control, (2) 1 mM melatonin treatment, (3) FSS, and (4) combined 1 mM melatonin and FSS. All groups had a fixed duration time of 2 hours. ERK, p-ERK, COX-2, $C/EBP{\beta}$, $PPAR{\gamma}$, osteopontin, Bax, caspase-3 and caspase-8 proteins were assessed by Western blot analysis. GAPDH was used as a control. Results showed that combined melatonin and FSS treatment activated the ERK/MAPK pathway but not COX-2. Furthermore, combined melatonin and FSS treatment significantly decreased $C/EBP{\beta}$ and $PPAR{\gamma}$ compared to other groups. However, caspase-3 and caspase-8 did not result in significant changes. In summary, combined melatonin and FSS appears to have the potential to inhibit adipogenesis and treat obesity.

• 대한의용생체공학회:의공학회지
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• 제39권4호
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• pp.168-174
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• 2018

Adipocytes affect obesity through the regulation of lipid metabolism. Physical loading is an important regulator of fat tissue. There are ongoing in vitro studies inducing mechanotransduction on 3T3-L1 preadipocytes with mechanical stimulus in order to treat obesity by inhibiting adipogenesis and provoking cell death. In this study, our goal was to suggest a new therapy for obesity by investigating whether fluid shear stress (FSS) changes transcription factors on 3T3-L1 related with adipogenesis and cell death. FSS loading was applied to 3T3-L1 preadipocytes at 1Pa and 1Hz. After loading, bright field images were taken and an immunofluorescence assay was conducted to observe actin stress fiber formation. Western blot analysis was conducted to identify the activation of the ERK pathway as well as the adipogenic factors, which including C/EBPs and $PPAR{\gamma}$. The expression of osteopontin, a protein related to inflammation in adipose tissue, and cell death related factors, Bax, Bcl-2, and Beclin, were also measured. Results showed that FSS stimulated the formation of actin stress fibers in 3T3-L1 and also that the activation of C/EBPs decreased significantly when compared with the control group. $PPAR{\gamma}$ activation in the 2 hour FSS group was lower than the 1 hour FSS group, which implied that the results were time dependent. Additionally, there were no differences in the expression of cell death factors after FSS loading. In summary, similar to other fibroblasts, the formation of actin stress fibers induced by mechanotransduction may affect the differentiation of 3T3-L1, leading to inhibition of adipogenesis and inflammation.