## 1 Introduction  
In mammals, adipose tissues are classified into three types: white adipose tissues (WAT), brown adipose tissues (BAT), and brown-like (beige or brite) adipose tissues. Each is composed of diverse morphological and physiological adipocyte communities [1]. WAT generally stores energy as triglycerides (TG), whereas the BAT and beige adipose tissues burn energy by uncoupling protein 1 (UCP1)-mediated thermogenesis. Morphologically, white adipocytes have single large lipid droplets and a small number of mitochondria, while the brown and beige adipocytes have multilocaler lipid droplets and large numbers of mitochondria. Both the brown and beige adipocytes express UCP1, a key thermogenic marker. They are physiologically and morphologically similar [1, 2]. However, they can be distinguished into different cell types based on their developmental properties. The brown adipocytes develop from Myf5-positive progenitors, whereas the beige adipocytes form in WAT depots and derive from a variety of origins depending on the depot [3, 4]. In particular, beige adipocytes can be activated within many WAT depots by cold exposure or \(\beta\)-adrenergic stimuli, thus exhibiting a higher degree of thermogenic plasticity. Thisprocess is known as browning (or beiging) [5; 6; 7]. Because BAT is rarely present in adult humans, the browning of the white adipocytes could be an attractive strategy to combat obesity and metabolic disorders [8]. UCP1-mediated thermogenesis can uncouple the ATP synthesis and control the proton concentration, producing heat in mitochondrial respiration [2]. The presence of UCP1 in the inner mitochondrial membrane reveals that mitochondria are essential organelles in beige adipocytes [6]. These organelles go through a sequence of dynamic processes, including degradation, biogenesis, fusion, and fission. Mitochondrial biogenesis increases mitochondrial volume density, as observed in BAT and the browning of WAT [9]. Mitochondrial fusion and fission can regulate mitochondrial morphology and quality [10]. Fusion is associated with mitofusins (MFN1 and MFN2) and optic atrophy 1 (OPA1), whereas fission is regulated by dynamin-related protein 1 (DRP1). MFN2 deletion in adipose tissues can reduce thermogenesis, however, it can protect against a high-fat diet [11; 12]. In addition, it has been reported that OPA1 can promote the browning of WAT [13]. The dynamic modification of mitochondrial shape and morphology can affect mitochondrial function. In patients with obesity and type 2 diabetes (T2D), it has been observed that mitochondrial fusion is decreased, but that fission is increased, indicating that an abnormal mitochondrial morphology is linked to the development of obesity-related metabolic disorders [14; 15]. As such, it is very important to balance the mitochondrial biogenesis and dynamics in the thermogenesis of beige adipocytes. Mitochondrial degradation is promoted by mitophagy, a type of autophagy. Mitophagy plays a key role in mitochondrial quality control, which involves the degradation of defected or redundant mitochondria through a selective pathway [16; 17]. When thermogenic stimuli are removed, beige adipocytes activate mitophagy and return to a white adipocyte phenotype [18; 19]. Mitophagy is initiated and regulated by PTEN-induced kinase 1 (PINK1) and Parkin in defected or redundant mitochondria [20]. The accumulation of PINK1 in the outer membrane of mitochondria (OMM) induces the phosphorylation of Parkin and results in the ubiquitination of OMM proteins, leading to mitophagy [21; 22]. There are several translocases in OMM, including the channel-forming protein, TOM40, for protein transport into mitochondria, and the sorting and assembly machinery (SAM) for membrane integration and assembly [23]. A member of the SAM complex, SAMM50, is essential for mitochondrial membrane organization and respiratory complex assembly, regulating cristae stability by interacting with the mitochondrial contact site and cristae organizing system complex [24; 25; 26].