Fasting induced fat oxidation is the physiological process where a period of nutrient abstinence triggers the preferential breakdown and utilization of stored body fat as the primary fuel source for energy production. This metabolic shift is a core component of metabolic flexibility and a necessary survival mechanism, ensuring energy supply when external nutrients are unavailable. Clinically, enhancing this capacity is a major therapeutic target for improving body composition and managing insulin resistance. The efficiency of this process reflects the body’s ability to transition smoothly between fed and fasted states.
Origin
This term is rooted in nutritional biochemistry and metabolic physiology, combining “fasting,” the stimulus, with “induced fat oxidation,” the resulting metabolic action. The recognition of fat as a primary fuel during periods of caloric restriction is a long-standing principle in human metabolism. Research into intermittent fasting and time-restricted eating has brought this concept to the forefront of wellness and clinical practice.
Mechanism
As circulating glucose and insulin levels drop during a fast, the anti-lipolytic signal of insulin diminishes, and the secretion of lipolytic hormones, such as glucagon and catecholamines, increases. This hormonal milieu activates hormone-sensitive lipase (HSL) in adipocytes, leading to the hydrolysis of triglycerides into free fatty acids and glycerol. These free fatty acids are then transported to tissues, including muscle and liver, where they undergo beta-oxidation within the mitochondria to generate ATP. In the liver, a portion of these fatty acids is converted into ketone bodies, an alternative fuel source for the brain.
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