[Research advances on the influence of poor dietary habits on the development of keloids]

Zhonghua Shao Shang Yu Chuang Mian Xiu Fu Za Zhi. 2022 Apr 20;38(4):389-393. doi: 10.3760/cma.j.cn501120-20210401-00112.
[Article in Chinese]

Abstract

Long-term poor dietary habits can cause changes in the intestinal flora, resulting in the production of a large number of lipopolysaccharide, increase intestinal mucosal permeability, and activate the entrance of a large number of inflammatory factors into the portal vein. In addition, a high carbohydrate diet can increase liver metabolic burden, increase mitochondrial oxidative phosphorylation, leading to oxidative stress, generate new fat during adenosine triphosphate synthesis, and thus resulting in ectopic fat accumulation, which further activate nuclear factor-κB signaling pathway and release inflam- matory factors such as tumor necrosis factor-α, interleukin-1β (IL-1β), IL-6, and so on. This leads to obesity and insulin resis- tance, ultimately triggering systemic low-grade inflammation. This article reviews the mechanism of poor dietary habits leading to systemic low-grade inflammation, the clinical and experimental research progress of keloids and systemic low-grade inflammation, the association between dietary habits and keloid constitution, and puts forward the hypothesis that poor dietary habits may lead to the occurrence and development of keloids.

长期的不良饮食习惯可造成肠道菌群改变,使得内毒素/脂多糖大量生成,导致肠道黏膜通透性增加,激活大量炎症因子进入门静脉。此外,高碳水化合物饮食可增加肝脏代谢负担,促进线粒体氧化磷酸化,导致氧化应激,在ATP合成过程中产生新的脂肪,从而导致脂肪异位堆积,激活核因子κB信号通路,释放肿瘤坏死因子α、白细胞介素1β(IL-1β)和IL-6等炎症因子,导致肥胖和胰岛素抵抗,最终引发系统性低度炎症。该综述回顾了不良饮食习惯导致系统性低度炎症的机制、瘢痕疙瘩与系统性低度炎症的临床研究与实验研究进展、饮食习惯与瘢痕疙瘩体质的关联性,提出了不良饮食习惯可能导致瘢痕疙瘩发生与发展的假说。.

Publication types

  • Review

MeSH terms

  • Diet* / adverse effects
  • Feeding Behavior
  • Humans
  • Inflammation / etiology
  • Inflammation / immunology
  • Inflammation / metabolism
  • Keloid* / etiology
  • Keloid* / immunology
  • Keloid* / physiopathology
  • NF-kappa B / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • NF-kappa B
  • Tumor Necrosis Factor-alpha