Abstract

Adipogenesis is a crucial cellular process that contributes to the expansion of adipose tissue in obesity. Shockwaves are mechanical stimuli that transmit signals to cause biological responses. The purpose of this study is to evaluate the effects of shockwaves on adipogenesis. We treated 3T3L-1 cells and human primary preadipocytes for differentiation with or without shockwaves. Western blots and quantitative real-time reverse transcriptase PCR (qRT-PCR) for adipocyte markers including peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT-enhancer-binding proteins (C/EBPα) were performed. Extracellular adenosine triphosphate (ATP) and intracellular cyclic adenosine monophosphate (cAMP) levels, which are known to affect adipocyte differentiation, were measured. Shockwave treatment decreased intracellular lipid droplet accumulation in primary human preadipocytes and 3T3-L1 cells after 11–12 days of differentiation. Levels of key adipogenic transcriptional factors PPARγ and/or C/EBPα were lower in shockwave-treated human primary preadipocytes and 3T3L-1 cells after 12–13 days of differentiation than in shockwave-untreated cells. Shockwave treatment induced release of extracellular ATP from preadipocytes and decreased intracellular cAMP levels. Shockwave-treated preadipocytes showed a higher level of β-catenin and less PPARγ expression than shockwave-untreated cells. Supplementation with 8-bromo-cAMP analog after shockwave treatment rescued adipocyte differentiation by preventing the effect of shockwaves on β-catenin, Wnt10b mRNA, and PPARγ expression. Low-energy shockwaves suppressed adipocyte differentiation by decreasing PPARγ. Our study suggests an insight into potential uses of shockwave-treatment for obesity.

Highlights

  • Adipose tissue regulates energy and metabolic homeostasis in the body

  • adenosine triphosphate (ATP) were added to 3T3-L1 cells instead of shockwave treatment

  • Extracorporeal shockwave treatment was introduced for lithotripsy in the 1980s [33,34]

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Summary

Introduction

Adipose tissue regulates energy and metabolic homeostasis in the body. White adipose tissue is a fat-storage organ for energy and an endocrine organ for secretion of adipokines including leptin, adiponectin, resistin, and other factors [1]. Adipose tissue is composed of adipocytes, adipose stem cells, and other cell types including vascular smooth muscle cells, endothelial and neuronal cells [2]. Among these cells, adipocytes generated through adipogenesis are the main component of adipose tissue. Adipogenesis is the process of commitment of mesenchymal stem cells (MSCs) to preadipocytes and achievement of terminal differentiation through which preadipocytes gain characteristics of mature adipocytes [3]. The major adipogenic transcriptional factors are peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT-enhancer-binding proteins (C/EBPs), which induce mature adipogenic phenotypes such as

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