Adipose tissue sensitivity describes the responsiveness of fat cells (adipocytes) to circulating hormones, particularly insulin and catecholamines, which dictates their function in energy storage and release. High sensitivity allows for efficient and regulated uptake of glucose and lipids, promoting metabolic health. Conversely, reduced sensitivity, often termed insulin resistance in adipose tissue, leads to dysregulated fat metabolism and contributes to systemic metabolic dysfunction. This measure is a critical indicator of overall metabolic flexibility and wellness.
Origin
This physiological concept is rooted in endocrinology and metabolism, stemming from the discovery of hormone receptors on adipocytes and their role in whole-body energy homeostasis. The term acknowledges adipose tissue not merely as a passive storage depot but as a dynamic endocrine organ itself. Its clinical relevance has grown with the understanding of obesity and type 2 diabetes pathogenesis. The ability of fat cells to respond appropriately to signals is essential for energy balance.
Mechanism
The mechanism revolves around the density and post-receptor signaling efficiency of key hormone receptors on the adipocyte membrane, such as the insulin receptor and beta-adrenergic receptors. Insulin binding triggers a cascade that facilitates glucose uptake via GLUT4 translocation and suppresses lipolysis. Impaired signaling within this pathway disrupts the delicate balance between lipogenesis (fat storage) and lipolysis (fat breakdown). This dysregulation contributes to chronic low-grade inflammation and altered adipokine secretion, driving systemic insulin resistance.
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