Purpose: Thermogenesis function has made brown/beige adipocyte an attractive target for obesity. Human brown adipose tissue activity is impaired in obesity in vivo. The present study aims to compare the differences in beige adipocyte differentiation potential of subcutaneous adipose tissue derived from normal weight and obese Chinese individuals in vitro. Methods: Adipose-derived stem cells (ADSCs) isolated from subcutaneous fat tissues of normal weight (NW) and obese (OB) groups were induced to differentiate into mature adipocyte with white adipocyte (WA)-and beige adipocyte (BA)-induction treatment. The expression of beige adipocyte marker protein UCP-1 and specific thermogenic genes was detected in differentiated adipocytes via Western blot and rt PCR, and the adipocyte mitochondrial function and lipolysis ability were also measured by oxygen consumption rate (OCR) and glycerol release rate, respectively. Results: Either with WA-induction or BA-induction, the expression of UCP-1 and beige adipo-cyte-specific thermogenic genes in differentiated adipocytes was higher in the NW compared to the OB group, followed by higher OCR and lipolysis ability in NW group than OB group. With BA-induction, expression of UCP-1 and thermogenic genes increased significantly, followed by the increasement in adipocytes OCR and lipolysis rate in NW group compared with WA-induction treatment, but no significant difference was observed in OB group. Conclusion: Compromised beige adipocyte differentiation plasticity was found in subcutaneous white adipose tissue derived from obese Chinese individuals, which may be due part to the downregulation of β3-adrenergic receptor expression in adipocytes. Discovery of ther-apeutic agents to active brown adipose tissue through specific pathways could provide a promising approach for treating obesity in the future.
CITATION STYLE
Li, H., Shen, L., Zhang, L., Yan, B., Sun, T., Guo, F., & Yin, X. (2020). Reduced beige adipogenic potential in subcutaneous adipocytes derived from obese Chinese individuals. Diabetes, Metabolic Syndrome and Obesity, 13, 2551–2562. https://doi.org/10.2147/DMSO.S248112
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