## 1 Introduction  
Adipose tissue serves a crucial role in maintaining overall metabolic balance, insulin sensitivity, and immune modulation. It acts as a storage site for excess fatty acids, preventing their accumulation in other organs and the associated negative consequences, such as steatosis and lipotoxicity [1]. Ageing is associated with the progressive deterioration of cellular function and is one of the greatest risk factors for developing a large cohort of debilitating diseases [2]. Age-associated insulin resistance, a prevalent metabolic disorder, affects a significant portion of the elderly population in the United States, leading to increased mortality rates, reduced functional status, higher hospitalization risk, and a substantial burden on healthcare systems [3]. Although the connection between obesity and diabetes is well-established, the relationship between aging and type 2 diabetes remains less understood [4] In fact, the correlation between declining glucose tolerance and aging was first observed nearly a century ago in 1921 [5]. Since then, numerous studies have identified reduced insulin sensitivity as the primary contributor to age-related impairments in glucose metabolism [6; 7]. Adipose tissue can be categorized into two main depots based on its anatomical localization: subcutaneous and visceral depots. The insulin sensitivity of these depots differs, with subcutaneous adipose tissue displaying higher sensitivity to insulin compared to the more insulin-resistant visceral depot [8]. The gradual loss of subcutaneous adipose tissue volume associated with aging leads to diminished glucose and lipid uptake, resulting in a phenomenon known as \"lipid overflow\" and the ectopic deposition of lipids in muscles and liver. This contributes to the development of insulin resistance [9]. Compprising various cell types, adipose tissue can be enzymatically digested to yield two primary fractions: the adipocyte fraction and the stromal vascular fraction (SVF) [10]. The SVF consists of adipose-derived stem cells (ASCs), lymphocytes, endothelial cells, pericytes, and fibroblasts [11]. ASCs are characterized by their immune-phenotypic profile as CD34 + CD90 + CD29 + CD45-CD31- cells of mesenchymal origin, possessing the ability to differentiate into adipocytes, as well as bone and cartilage cells [12; 13]. In white adipose tissue, these cells predominantly reside in the vascular stroma surrounding small blood vessels, where they can undergo proliferation and adipogenic differentiation [12]. At the transcriptional level, the primary regulators of adipogenesis are the key transcription factors peroxisome proliferatorator-activated receptor \(\gamma\) (PPAR\(\gamma\)), CCAAT/enhancer binding protein \(\alpha\) (C/EBP\(\alpha\)) and CCAAT/enhancer binding protein \(\beta\)[14]. These transcription factors play essential roles in inducing growth arrest and orchestrating the sequential expression of genes involved in lipid metabolism. Notably, they regulate the expression of key adipocyte-specific hormones such as adiponectin and leptin. ASCs play a crucial role in adipose tissue regeneration through their capacity for proliferation, self-renewal, and differentiation. However, aging is associated with a decline in the stemness properties of ASCs [15; 16]. The age-related reduction in subcutaneous fat depot size is thought to be influenced by alterations in the replication and differentiation capabilities of ASCs [17; 18; 19]. Accumulation of oxidative stress within adipose tissue during aging has been proposed as a contributing factor that negatively affects the differentiation capacity of ASCs [17]. Nevertheless, the exact mechanisms underlying the loss of stemness in ASCs during aging remain unclear. Recent studies have highlighted a connection between decreased autophagy, increased mechanistic targets of rapamycin (mTOR) pathway activity, and the accumulation of reactive oxygen species (ROS) with the loss of stemness and premature senescence induction in ASCs [20; 21; 22].