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餐后代谢紊乱及其医学影响。

Postprandial Dysmetabolism and Its Medical Implications.

作者信息

Sasso Emanuel, Baticic Lara, Sotosek Vlatka

机构信息

Faculty of Medicine, University of Rijeka, Brace Branchetta 20, 51000 Rijeka, Croatia.

Department of Medical Chemistry, Biochemistry and Clinical Chemistry, Faculty of Medicine, University of Rijeka, Brace Branchetta 20, 51000 Rijeka, Croatia.

出版信息

Life (Basel). 2023 Dec 10;13(12):2317. doi: 10.3390/life13122317.


DOI:10.3390/life13122317
PMID:38137918
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10744591/
Abstract

An unbalanced diet increases the risk of developing a variety of chronic diseases and cancers, leading to higher morbidity and mortality rates worldwide. Low-grade systemic chronic inflammation mediated by the activation of the innate immune system is common to all these pathologies. Inflammation is a biological response of the body and a normal part of host defense to combat the effects of bacteria, viruses, toxins and macronutrients. However, when the innate immune system is constantly activated, it can promote the development of low-grade systemic chronic inflammation, which could play an important role in the development of chronic diseases and cancer. Since most chronic inflammatory diseases are associated with diet, a balanced healthy diet high in anti-inflammatory food components could prevent chronic diseases and cancer. The cells of the body's immune system produce chemokines and cytokines which can have pro-inflammatory and tumor-promoting as well as anti-inflammatory and tumor-fighting functions. A challenge in the future will be to assess whether polymorphisms in immune-related genes may play a role in promoting pro-inflammatory activity. Thanks to this duality, future research on immune regulation could focus on how innate immune cells can be modified to convert a pro-inflammatory and tumor-friendly microenvironment into an anti-inflammatory and anti-tumor one. This review describes inflammatory responses mediated by the innate immune system in various diseases such as hyperglycemia and/or hyperlipemia, obesity, type II diabetes, cardiovascular disease and cancer.

摘要

不均衡的饮食会增加患多种慢性疾病和癌症的风险,导致全球发病率和死亡率上升。由先天免疫系统激活介导的低度全身性慢性炎症是所有这些疾病的共同特征。炎症是身体的一种生物学反应,是宿主防御细菌、病毒、毒素和大量营养素影响的正常组成部分。然而,当先天免疫系统持续被激活时,它会促进低度全身性慢性炎症的发展,而这可能在慢性疾病和癌症的发展中起重要作用。由于大多数慢性炎症性疾病都与饮食有关,富含抗炎食物成分的均衡健康饮食可以预防慢性疾病和癌症。人体免疫系统的细胞会产生趋化因子和细胞因子,它们具有促炎和促进肿瘤生长以及抗炎和抗癌的功能。未来的一个挑战将是评估免疫相关基因的多态性是否可能在促进促炎活性中起作用。由于这种双重性,未来关于免疫调节的研究可能会集中在如何对先天免疫细胞进行改造,以将促炎和有利于肿瘤的微环境转变为抗炎和抗癌的微环境。这篇综述描述了先天免疫系统在高血糖和/或高血脂、肥胖、II型糖尿病、心血管疾病和癌症等各种疾病中介导的炎症反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6de9/10744591/b1e568aa9d21/life-13-02317-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6de9/10744591/03b1c3f20545/life-13-02317-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6de9/10744591/527417d17ac6/life-13-02317-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6de9/10744591/24e377e43b60/life-13-02317-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6de9/10744591/5f0ae26842db/life-13-02317-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6de9/10744591/b1e568aa9d21/life-13-02317-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6de9/10744591/03b1c3f20545/life-13-02317-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6de9/10744591/527417d17ac6/life-13-02317-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6de9/10744591/24e377e43b60/life-13-02317-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6de9/10744591/5f0ae26842db/life-13-02317-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6de9/10744591/b1e568aa9d21/life-13-02317-g005.jpg

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引用本文的文献

[1]
A sensitive bioassay to measure NOD1/2 ligands in human serum reveals differential postprandial NOD2 activation.

Front Nutr. 2025-6-25

[2]
Dynamic profiling of Cell-free DNA fragmentation uncovers postprandial metabolic and immune alterations.

Hum Genomics. 2025-3-18

[3]
Impaired postprandial GLP-2 response enhances endotoxemia, systemic inflammation, and kidney injury in metabolic dysfunction-associated steatohepatitis (MASH): effect of phospholipid curcumin meriva.

Gut Microbes. 2024

本文引用的文献

[1]
Microbiota and IBD: Current knowledge and future perspectives.

Dig Liver Dis. 2024-6

[2]
Nutrigenomics: SNPs Correlated to Lipid and Carbohydrate Metabolism.

Clin Ter. 2023

[3]
Take-Home Messages from 20 Years of Progress in Dietary Therapy of Inflammatory Bowel Disease.

Ann Nutr Metab. 2023

[4]
The Impact and Burden of Dietary Sugars on the Liver.

Hepatol Commun. 2023-11-1

[5]
Metabolic-Dysfunction-Associated Steatotic Liver Disease-Its Pathophysiology, Association with Atherosclerosis and Cardiovascular Disease, and Treatments.

Int J Mol Sci. 2023-10-23

[6]
Dietary biomarkers-an update on their validity and applicability in epidemiological studies.

Nutr Rev. 2024-9-1

[7]
Identification of adipose tissue transcriptomic memory of anorexia nervosa.

Mol Med. 2023-8-15

[8]
Novel therapeutic approaches based on the pathological role of gut dysbiosis on the link between nonalcoholic fatty liver disease and insulin resistance.

Eur Rev Med Pharmacol Sci. 2023-3

[9]
Inflammation in obesity, diabetes, and related disorders.

Immunity. 2022-1-11

[10]
Innate Immunity and Cancer Pathophysiology.

Annu Rev Pathol. 2022-1-24

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