Relationship between Dietary Nutrient Intake and Autophagy–Related Genes in Obese Humans. A Narrative Review

Obesity is one of the world's major public health challenges. Its pathogenesis and comorbid metabolic disorders share common mechanisms, such as mitochondrial or endoplasmic reticulum dysfunction or oxidative stress, gut dysbiosis, chronic in-flammation and altered autophagy. Numerous pro-autophagy dietary interventions are being investigated for their potential obesity-preventing or therapeutic effects. In this review, we summarize current data on the relationship between autophagy and obesity and discuss various non-pharmacological dietary interventions as regu-lators of autophagy-related genes in the prevention and ultimately treatment of obe-sity in humans, available in scientific databases and published through July 2024. Lifestyle modification (such as calorie restriction, intermittent fasting, physical exer-cise), a diet rich in flavonoids, antioxidants, specific fatty acids, specific amino acids and others have shown a beneficial role in the induction of this process. Induction of autophagy by heterogeneous interventions elicits a relatively homogeneous response characterized by activation of specific kinases (AMPK, IKK, JNK1, TAK1, ULK1, VPS34), inhibition of others (such as mTORC1), protein deacetylation reactions (at least in part providing SIRT1 activation and/or EP300 inhibition), and reversal of in-hibitory interactions such as those between BECN1 and members of the Bcl-2 family.