Catabolic Hormone Signaling refers to the cascade of molecular events initiated by hormones whose principal action is to break down complex storage molecules into simpler substrates, such as glucose and amino acids, to mobilize energy. Key examples include cortisol, glucagon, and adrenaline, which are essential for survival during periods of stress, fasting, or acute energy deficit. While crucial for acute adaptation, chronic or excessive signaling in this pathway leads to the detrimental degradation of essential tissues, notably muscle and bone.
Origin
This term is a core concept in endocrinology and metabolism, derived from the Greek word katabolē, meaning “a throwing down” or degradation. It is the physiological opposite of anabolic signaling, which focuses on synthesis and building. The clear distinction between these two opposing hormonal forces is fundamental to understanding energy balance and tissue homeostasis in human physiology.
Mechanism
Catabolic hormones bind to their specific cell-surface or intracellular receptors, triggering pathways that activate degradative enzymes within the target cell. For instance, cortisol signaling upregulates the ubiquitin-proteasome system in skeletal muscle, promoting the breakdown of structural proteins into amino acids for hepatic gluconeogenesis. Glucagon, conversely, primarily targets the liver to promote glycogenolysis and the release of stored glucose. The coordinated effect is the rapid provision of metabolic fuel at the expense of tissue integrity.
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