Абстракт

Objectives: To explain the metabolic shift occurring during 24–36 hour fasting, including glycogen depletion, ketogenesis, and hormonal adaptations. To describe the molecular pathways involved, particularly AMPK activation, mTOR inhibition, IGF-1 modulation, and their relationship with autophagy. To analyze the role of fasting in mitochondrial biogenesis and metabolic flexibility. To evaluate current clinical evidence regarding insulin sensitivity, visceral fat reduction, inflammation, and chronic metabolic disease risk. Introduction: Deep fasting lasting 24–36 hours has emerged as a metabolic intervention with potential relevance in the prevention and modulation of chronic diseases. During this period, a metabolic shift occurs characterized by hepatic glycogen depletion, decreased insulin levels, increased glucagon secretion, and activation of energy-sensing pathways such as AMPK, with concomitant inhibition of mTOR. This transition promotes ketogenesis, elevation of beta-hydroxybutyrate, and improved metabolic flexibility. Materials / method: From a clinical perspective, these mechanisms are associated with improved insulin sensitivity, reduction in visceral adiposity, lower inflammatory markers, and a potential decrease in the risk of chronic metabolic diseases, including type 2 diabetes, metabolic syndrome, and cardiovascular disease. Preclinical evidence also suggests a possible protective role in oncologic risk modulation through differential metabolic stress mechanisms, although robust human data remain limited. Results: Implementation of 24–36 hour fasting protocols demonstrates a reproducible metabolic transition characterized by decreased circulating insulin and IGF-1, increased lipolysis, and significant elevation of beta-hydroxybutyrate levels. This metabolic shift correlates with activation of AMPK and suppression of mTOR signaling, promoting cellular conditions associated with autophagy and improved metabolic efficiency. Human clinical studies report improved insulin sensitivity, reductions in visceral adiposity, modest decreases in inflammatory markers, and enhanced metabolic rate Conclusion: In conclusion, 24–36 hour deep fasting represents a metabolic strategy capable of activating cellular programs linked to longevity and metabolic resilience. Long-term randomized controlled trials are needed to establish efficacy, safety, and optimal implementation protocols in specific populations.