This describes the sensitivity and capacity of the body’s tissues, particularly the liver and peripheral cells, to react appropriately to signals within the somatotropic axis, specifically Growth Hormone (GH) and Insulin-like Growth Factor 1 (IGF-1). Responsiveness is a measure of the system’s ability to translate a GH signal into a proportional biological effect, such as protein synthesis or lipolysis. A decline in this responsiveness, often seen with age or obesity, diminishes the restorative and metabolic effects of the hormone.
Origin
The term is derived directly from endocrinology, combining “Growth Hormone Axis,” referring to the hypothalamic-pituitary-somatotropic signaling cascade, with “Responsiveness,” a clinical measure of biological efficacy. The axis is a fundamental system in human physiology, regulating growth in youth and metabolism/repair in adulthood. Diminished responsiveness is a key feature of somatopause.
Mechanism
The core mechanism involves GH binding to its receptor on hepatocytes, stimulating the production of IGF-1, which then acts as the primary mediator of anabolic effects in peripheral tissues. Responsiveness can be impaired by chronic inflammation or excess visceral fat, which interfere with GH receptor signaling or post-receptor kinase cascades. Clinical strategies aim to improve this sensitivity by addressing underlying metabolic dysfunction.
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