Version 1
: Received: 4 November 2023 / Approved: 6 November 2023 / Online: 7 November 2023 (07:10:30 CET)
How to cite:
Kwon, S. J.; Khan, M. S.; Kim, S. G. Dual Impact of Dietary Lipids on Inflammatory Bowel Disease: A Two-Edged Sword. Preprints2023, 2023110366. https://doi.org/10.20944/preprints202311.0366.v1
Kwon, S. J.; Khan, M. S.; Kim, S. G. Dual Impact of Dietary Lipids on Inflammatory Bowel Disease: A Two-Edged Sword. Preprints 2023, 2023110366. https://doi.org/10.20944/preprints202311.0366.v1
Kwon, S. J.; Khan, M. S.; Kim, S. G. Dual Impact of Dietary Lipids on Inflammatory Bowel Disease: A Two-Edged Sword. Preprints2023, 2023110366. https://doi.org/10.20944/preprints202311.0366.v1
APA Style
Kwon, S. J., Khan, M. S., & Kim, S. G. (2023). Dual Impact of Dietary Lipids on Inflammatory Bowel Disease: A Two-Edged Sword. Preprints. https://doi.org/10.20944/preprints202311.0366.v1
Chicago/Turabian Style
Kwon, S. J., Muhammad Sohaib Khan and Sang Geon Kim. 2023 "Dual Impact of Dietary Lipids on Inflammatory Bowel Disease: A Two-Edged Sword" Preprints. https://doi.org/10.20944/preprints202311.0366.v1
Abstract
Inflammatory bowel diseases (IBD), including Crohn's disease and ulcerative colitis, is a disease of chronic inflammatory conditions of the intestinal tract due to disturbance of the inflammation and immune system. Symptoms of IBD include abdominal pain, diarrhea, bleeding, reduced weight, and fatigue. In IBD, the immune system attacks the intestinal tract's inner wall, causing chronic inflammation and tissue damage. In particular, IL-6 and IL-17 act on immune cells, including T cells and macrophages, to amplify the immune responses so that tissue damage and morphological changes occur. Of note, excessive calorie intake and obesity also affect the immune system due to inflammation caused by lipotoxicity and changes in lipids supply. Similarly, individuals with IBD have alterations in liver function after sustained high-fat diet feeding. In addition, excess dietary fat intake, along with alterations in primary and secondary bile acids in the colon, can affect the onset and progression of IBD because inflammatory cytokines contribute to insulin resistance; the factors include the release of inflammatory cytokines, oxidative stress, and changes in intestinal microflora, which may also contribute to the disease progression. However, interfering with de novo fatty acid synthase by deleting the enzyme acetyl-CoA-carboxylase 1 in intestinal epithelial cells leads to the deficiency of epithelial crypt structures and tissue regeneration, which seems to be due to Lgr5+ intestinal stem cell function. Thus, conflicting reports exist regarding high-fat diet effects on IBD animal models. This review will focus on the pathological basis of the link between dietary lipids intake and IBD and cover currently available pharmacological approaches.
Keywords
IBD; IECs; Lipid intake; Stem cells; Inflammation
Subject
Biology and Life Sciences, Biochemistry and Molecular Biology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
