Bednarczyk Martyna, Dąbrowska-Szeja Nicola, Łętowski Dariusz, Dzięgielewska-Gęsiak Sylwia, Waniczek Dariusz, Muc-Wierzgoń Małgorzata
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.
Nutrients. 2024 Nov 22;16(23):4003. doi: 10.3390/nu16234003.
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.
肥胖是全球主要的公共卫生挑战之一。其发病机制和合并的代谢紊乱具有共同的机制，如线粒体或内质网功能障碍、氧化应激、肠道菌群失调、慢性炎症和自噬改变。目前正在研究许多促进自噬的饮食干预措施对预防肥胖或治疗肥胖的潜在作用。我们总结了目前关于自噬与肥胖之间关系的数据，并讨论了各种饮食干预措施作为自噬相关基因的调节剂在预防和最终治疗人类肥胖中的作用，这些信息来自科学数据库以及截至2024年7月发表的文献。生活方式的改变（如热量限制、间歇性禁食、体育锻炼），包括遵循富含黄酮类化合物、抗氧化剂、特定脂肪酸、特定氨基酸等的饮食，已显示出在诱导这一过程中具有有益作用。通过各种营养干预激活自噬往往会引发一致的反应，其特征是诱导某些激酶（包括AMPK、IKK、JNK1、TAK1、ULK1和VPS34）或抑制其他激酶（如mTORC1）、蛋白质去乙酰化以及减轻BECN1与Bcl-2家族成员之间的抑制性相互作用。许多营养物质（营养保健品）的显著健康/转化特性可通过包括激活或抑制自噬在内的各种机制影响慢性病风险。营养干预在肥胖及其合并症中调节自噬的作用尚不清楚，尤其是在肥胖个体中。
