THE ROLE OF AUTOPHAGY IN THE PATHOGENESIS OF TYPE 2 DIABETES AND BIOCHEMICAL CORRECTION OF INTERVAL FASTING
Abstract
Metabolic dysfunction at the cellular level remains a key factor in the pathogenesis of type 2 diabetes mellitus (T2DM) worldwide. This article analyzes the blockade of the autophagy process as a result of excessive activation of the mTOR signaling pathway in conditions of chronic hyperinsulinemia. The study examines the possibilities of activating the AMPK protein and triggering the "metabolic switch" mechanism through the intermittent fasting (16:8) regime. The data show that 16–18 h of fasting biochemically corrects insulin resistance by breaking down amyloid aggregates in beta cells. The results obtained justify the advantages of a cytocentric approach in reducing the pharmacological burden in the control of T2DM and achieving disease remission.
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