## 3 Discussion  
The thermogenesis of brown/beige adipocytes plays an important role in the controlling energy balance in the treatment of obesity and metabolic disorders [8; 29]. The location of UCP1 in the inner mitochondrial membrane suggests that the mitochondrion is an important cytoplasmic organelle for the thermogenesis of brown/beige adipocytes [6]. Mitochondrial properties exert a reversible effect on the metabolism and energy balance of cells overall. Therefore, quality control, regulated through the mitochondrial dynamics of movement, fusion, and fission, is essential [30]. Moreover, mitochondrial dynamics are reported to play a role in maintaining electrical and biochemical connectivity, modulating metabolic efficiency, protecting mitochondrial DNA, regulating apoptosis, and interacting with other cellular organelles [30]. Additionally, mitochondrial morphology acts as the consequence of a balance between fission and fusion activities [30], and it has been reported that the regulation of morphology and energy metabolism through mitochondrial dynam  
Figure 6: The effects of SAMM50 knockdown and overexpression on the thermogenesis of beige adipocytes. (**A,B**) The expression levels of thermogenic genes in beige adipocytes infected with shSAMM50 (**A**) and FLAG-tagged SAMM50 (**B**) were analyzed by qPCR analysis. (**C,D**) Western blot analysis was performed to determine the protein levels of PPARGC1A and UCP1 in the shSAMM50 (**C**) and FLAG-tagged SAMM50 (**D**) -infected beige adipocytes. The protein levels of PPARGC1A and UCP1 were quantified using ImageJ software. Results are shown as mean \(\pm\) SEM. * \(p\) < 0.05; **_p_ < 0.01; ***_p_ < 0.005 compared to the controls. ics is related to the thermogenesis of brown/beige adipocytes [31]. The mitochondrial dynamics that regulate thermogenesis involve not only the respiratory complex assembly and production of ROS, but additionally, the modulation of mitochondria interaction with intracellular organelles (endoplasmic reticulum and lipid droplets) [31; 32]. Therefore, several studies have shown that the balancing of the mitochondrial dynamics has the potential to regulate the thermogenesis of beige adipocytes [31]. Generally, beige adipocytes are characterized by the high expression of UCP1 [2], and additionally, the gene expression of _PPARGC1A_, _DIO2_, _ELOVL3_, _CIDEA_, and _CIDEC_ has been reported as a biomarker for thermogenic activity [2; 6]. Particularly, PPARGC1A acts as a transcriptional key regulator of thermogenesis through the regulation of mitochondrial biogenesis, which is involved in the initialization of adipocyte browning [3]. As biomarkers determine beige adipocytes, the expression of genes, such as _PAT2_, _SLC25A20_, _FABP3_, _PDK4_, and _CITED1_ has been observed [2; 33; 34; 33]. In this study, the differentiation of hADSCs into beige adipocytes was established. Additionally, lipid accumulation and adipogenic markers, _CEBPA_, _PPARG_, _ADIPOQ_, and _FASN_ were significantly increased in both the white and beige adipogenic differentiation of hADSCs when compared with the undifferentiated hADSCs (Figure 1B,C). Similarly, the expression of thermogenic and beige-specific genes, including UCP1, significantly increased in the beige group when compared with the white and hADSC group, confirming the differentiation of hADSCs into beige adipocytes (Figure 2A,C). Another characteristic feature of beige adipocytes is their active metabolic function through a high mitochondrial concentration [6]. Specifically, mitophagy can induce mitochondrial degradation through PINK1-Parkin-mediated autophagy [20]. Moreover, recent studies have shown that mitophagy is involved in the conversion of beige adipocytes to white adipocytes in humans [19]. Recently, SAMM50 has been reported as a key regulator of PINK1-Parkin-mediated mitophagy and mitochondrial dynamics [28]. Based on all of these findings, it was hypothesized that SAMM50 could regulate the mitochondrial dynamics in the thermogenesis of beige adipocytes.