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Journal Article Review Epublish 3 citations

PubMed: 39683397 DOI: 10.3390/nu16234003

Relationship Between Dietary Nutrient Intake and Autophagy-Related Genes in Obese Humans: A Narrative Review.

Nutrients 16(23)

Authors: Martyna Bednarczyk, Nicola Dąbrowska-Szeja, Dariusz Łętowski, Sylwia Dzięgielewska-Gęsiak, Dariusz Waniczek, Małgorzata Muc-Wierzgoń

Affiliations

  • Department of Cancer Prevention, Faculty of Public Health, Medical University of Silesia in Katowice, 40-055 Katowice, Poland.
  • Department of Internal Diseases Propaedeutics and Emergency Medicine, Faculty of Public Health in Bytom, Medical University of Silesia in Katowice, 40-055 Katowice, Poland.
  • Department of Oncological Surgery, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, 40-055 Katowice, Poland.

Abstract

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 inflammation and altered autophagy. Numerous pro-autophagy dietary interventions are being investigated for their potential obesity-preventing or therapeutic effects. We summarize current data on the relationship between autophagy and obesity, and discuss various dietary interventions as regulators of autophagy-related genes in the prevention and ultimate treatment of obesity in humans, as available in scientific databases and published through July 2024. Lifestyle modifications (such as calorie restriction, intermittent fasting, physical exercise), including following 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. The activation of autophagy through various nutritional interventions tends to elicit a consistent response, characterized by the induction of certain kinases (including AMPK, IKK, JNK1, TAK1, ULK1, and VPS34) or the suppression of others (like mTORC1), the deacetylation of proteins, and the alleviation of inhibitory interactions between BECN1 and members of the Bcl-2 family. Significant health/translational properties of many nutrients (nutraceuticals) can affect chronic disease risk through various mechanisms that include the activation or inhibition of autophagy. The role of nutritional intervention in the regulation of autophagy in obesity and its comorbidities is not yet clear, especially in obese individuals.

MeSH

Nutrients, Exercise, Genes, Autophagy, Diet, Food, Obesity, Therapeutics, Overweight

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