This term describes the degree to which cellular androgen receptors respond to circulating androgens, such as testosterone and dihydrotestosterone. High sensitivity means a robust biological response is elicited even with lower hormone concentrations. Conversely, reduced sensitivity requires higher androgen levels to achieve the same physiological effect. The modulation of this receptor function is critical for maintaining tissue-specific hormonal effects across the body.
Origin
The concept combines the endocrinological term ‘androgen,’ referring to male sex hormones, and ‘receptor sensitivity,’ a fundamental principle in pharmacology and cellular biology. This idea emerged from the study of how steroid hormones exert their effects by binding to intracellular receptors that then translocate to the nucleus. Clinical understanding of androgen insensitivity syndromes solidified the importance of receptor function over merely hormone concentration.
Mechanism
Androgen receptor sensitivity is primarily regulated by genetic factors and post-translational modifications of the receptor protein. Once an androgen binds, the receptor complex initiates gene transcription, influencing protein synthesis and cellular function. Variations in co-regulator proteins, which enhance or suppress the receptor’s activity, directly determine the magnitude of the downstream cellular response in target tissues like muscle, bone, and skin.
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