Endocrinological aspects of sarcopenic obesity

Background: Sarcopenic obesity (SO) is a multifactorial condition characterized by the coexistence of excess adiposity and reduced skeletal muscle mass and function. Its development reflects a complex interaction of metabolic, inflammatory, and endocrine mechanisms that disrupt the balance between anabolic and catabolic processes. Main findings: Endocrine dysfunction is a major driver of the altered adipose–muscle crosstalk characteristic of SO. Hormonal imbalance amplifies mitochondrial dysfunction, oxidative stress, and chronic inflammation, leading to reduced muscle quality and increased visceral and intramuscular fat. Age-related hormonal decline, including reductions in testosterone and estrogens, growth hormone (GH), insulin-like growth factor 1, and thyroid hormones, together with increased catabolic activity of glucocorticoids and the renin–angiotensin–aldosterone system, as well as altered sympathoadrenal signaling, promotes insulin resistance, muscle catabolism, and fat accumulation. Beyond aging, endocrine diseases such as hypogonadism, GH deficiency, hypothyroidism, Cushing syndrome, hyperaldosteronism, and diabetes replicate many features of SO and serve as valuable models for investigating its underlying mechanisms. Future directions: Emerging anabolic or anti-catabolic agents, such as Selective Androgen Receptor Modulators (SARMs), myostatin inhibitors, and ghrelin analogues, show promise but require further validation. Future research should explore endocrine disorders as experimental models of SO, focusing on the shared molecular and hormonal mechanisms that link fat accumulation and muscle loss. Finally, studying endocrine pathways in an integrated manner, rather than focusing on obesity and sarcopenia separately, may identify new hormonal targets for precision therapies aimed at restoring anabolic–catabolic balance and improving metabolic and functional outcomes in individuals with SO.