A state in the circulatory system where the binding sites on specific transport proteins, such as Sex Hormone-Binding Globulin (SHBG) or Corticosteroid-Binding Globulin (CBG), are maximally occupied by their respective steroid hormones. This physiological condition dictates the proportion of free, biologically active hormone available to target tissues, a crucial factor in endocrine function. Clinically, saturation levels are critical for accurately interpreting total hormone measurements and managing replacement therapies.
Origin
This concept is fundamental to classical endocrinology, stemming from early biochemical studies on hormone transport and pharmacokinetics in the blood. The principle of protein binding and its effect on hormonal bioavailability is a core tenet of understanding steroid hormone action. It applies the principles of enzyme kinetics and ligand-receptor binding to the circulating hormone pool.
Mechanism
When the concentration of circulating hormones, such as testosterone or estradiol, exceeds the binding capacity of their carrier proteins, the unbound fraction—the “free hormone”—rises disproportionately. This increased free fraction is the active component that can diffuse across cell membranes and interact with intracellular receptors to exert its biological effect. Saturation therefore serves as a rate-limiting step for hormone action, significantly influencing the physiological impact of both endogenous production and exogenous administration.
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