The Energy Mobilization Cascade describes the sequential hormonal and enzymatic signaling events triggered by perceived energy deficit, leading to the release of stored substrates—glycogenolysis, lipolysis, and subsequent gluconeogenesis—to maintain systemic glucose homeostasis. This cascade is centrally regulated by counter-regulatory hormones like glucagon, epinephrine, and cortisol, working in opposition to insulin’s storage signal. Effective management of this cascade is vital for sustaining physical and cognitive function during periods of fasting or high demand. It is the body’s prioritized system for accessing fuel reserves.
Origin
This term is derived from intermediary metabolism and endocrinology, mapping the temporal sequence of fuel access pathways activated under catabolic conditions. The ‘cascade’ emphasizes the dependency of one step upon the successful initiation of the preceding hormonal signal. Clinically, understanding the cascade is key to differentiating between appropriate physiological mobilization and pathological states like uncontrolled diabetes or adrenal insufficiency.
Mechanism
Upon sensing low ATP or reduced nutrient availability, the hypothalamus signals the release of counter-regulatory hormones that activate adenylyl cyclase pathways in target tissues. This results in the phosphorylation and activation of key enzymes like hormone-sensitive lipase in adipocytes and glycogen phosphorylase in hepatocytes. Cortisol further sustains this state by promoting the synthesis of necessary enzymes for gluconeogenesis in the liver, ensuring a steady supply of circulating fuel substrates.
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