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生酮饮食的代谢效应:探究与脂肪组织和其他代谢器官相关的全身代谢。

Metabolic Effects of Ketogenic Diets: Exploring Whole-Body Metabolism in Connection with Adipose Tissue and Other Metabolic Organs.

机构信息

Department of Biology and Chemistry, Changwon National University, Changwon 51140, Republic of Korea.

出版信息

Int J Mol Sci. 2024 Jun 27;25(13):7076. doi: 10.3390/ijms25137076.

DOI:10.3390/ijms25137076
PMID:39000187
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11241756/
Abstract

The ketogenic diet (KD) is characterized by minimal carbohydrate, moderate protein, and high fat intake, leading to ketosis. It is recognized for its efficiency in weight loss, metabolic health improvement, and various therapeutic interventions. The KD enhances glucose and lipid metabolism, reducing triglycerides and total cholesterol while increasing high-density lipoprotein levels and alleviating dyslipidemia. It significantly influences adipose tissue hormones, key contributors to systemic metabolism. Brown adipose tissue, essential for thermogenesis and lipid combustion, encounters modified UCP1 levels due to dietary factors, including the KD. UCP1 generates heat by uncoupling electron transport during ATP synthesis. Browning of the white adipose tissue elevates UCP1 levels in both white and brown adipose tissues, a phenomenon encouraged by the KD. Ketone oxidation depletes intermediates in the Krebs cycle, requiring anaplerotic substances, including glucose, glycogen, or amino acids, for metabolic efficiency. Methylation is essential in adipogenesis and the body's dietary responses, with DNA methylation of several genes linked to weight loss and ketosis. The KD stimulates FGF21, influencing metabolic stability via the UCP1 pathways. The KD induces a reduction in muscle mass, potentially involving anti-lipolytic effects and attenuating proteolysis in skeletal muscles. Additionally, the KD contributes to neuroprotection, possesses anti-inflammatory properties, and alters epigenetics. This review encapsulates the metabolic effects and signaling induced by the KD in adipose tissue and major metabolic organs.

摘要

生酮饮食(KD)的特点是碳水化合物含量低、蛋白质含量适中、脂肪含量高,从而导致酮症。它在减肥、改善代谢健康和各种治疗干预方面都很有效。KD 增强了葡萄糖和脂质代谢,降低了甘油三酯和总胆固醇,同时提高了高密度脂蛋白水平并改善了血脂异常。它还显著影响了脂肪组织激素,这些激素是全身代谢的关键因素。棕色脂肪组织对产热和脂肪燃烧至关重要,而饮食因素,包括 KD,会导致其关键的解偶联蛋白 1(UCP1)水平发生变化。UCP1 通过在 ATP 合成过程中解偶联电子传递来产生热量。白色脂肪组织的褐变会提高白色和棕色脂肪组织中的 UCP1 水平,KD 会促进这一现象的发生。酮体氧化会消耗克雷布斯循环中的中间产物,这就需要包括葡萄糖、糖原或氨基酸在内的补充物质来维持代谢效率。甲基化在脂肪生成和身体对饮食的反应中至关重要,与体重减轻和酮症相关的几个基因的 DNA 甲基化就是一个例子。KD 会刺激成纤维细胞生长因子 21(FGF21)的产生,通过 UCP1 途径影响代谢稳定性。KD 会导致肌肉质量减少,这可能涉及到抗脂肪分解作用和减弱骨骼肌蛋白水解。此外,KD 还有助于神经保护、具有抗炎特性并改变表观遗传学。本综述总结了 KD 在脂肪组织和主要代谢器官中诱导的代谢效应和信号转导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c88c/11241756/092da9f51b2d/ijms-25-07076-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c88c/11241756/092da9f51b2d/ijms-25-07076-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c88c/11241756/092da9f51b2d/ijms-25-07076-g001.jpg

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