Cooperation of transposable elements to endow global networks of initiators of hybrid assembly pathways of endogenous multiprotein complexes.

Sarcopenia is a progressive skeletal muscle disorder. It is characterized by declines in muscle mass, strength, and physical performance. These declines increase the risks of disability, hospitalization, and mortality. Recent consensus statements from the Global Leadership Initiative in Sarcopenia (GLIS) and the Asian Working Group for Sarcopenia (AWGS) emphasize these domains as core diagnostic components and highlight that reductions in muscle mass may precede functional impairment (, ). Although traditionally age-related, sarcopenia is increasingly recognized as a common comorbidity of type 2 diabetes mellitus (T2DM), showing a substantially higher prevalence than in non-diabetic populations (, , ). Epidemiological studies indicate that the prevalence of sarcopenia in patients with T2DM is approximately two- to threefold higher than that in non-diabetic individuals, with reported rates reaching around 27.9% in older populations (, ).This association is driven by interrelated mechanisms, including insulin resistance, chronic inflammation, mitochondrial dysfunction, and advanced glycation end product accumulation, which impair muscle protein homeostasis. In turn, skeletal muscle loss further exacerbates insulin resistance, forming a bidirectional pathological cycle and contributing to adverse outcomes such as impaired physical function, increased fall risk, and higher cardiovascular and all-cause mortality (, ). Sodium-glucose transporter 2 (SGLT2) inhibitors are a cornerstone therapy for T2DM, recommended as first-line or early combination agents due to their glucose-lowering efficacy and established cardiovascular and renal benefits (, ). SGLT2 inhibitors induce glycosuria and a negative energy balance, leading to modest but sustained weight loss (). However, a key concern has emerged: does this weight loss come mainly from fat, or does it also reduce lean and skeletal muscle mass? The latter would potentially increase sarcopenia risk (). Conversely, other studies have demonstrated significant reductions in adiposity without corresponding losses in muscle mass or strength, indicating a neutral effect on muscle preservation (, ).