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Protaetia Brevitarsis-Derived Protein Hydrolysate Reduces Obesity-Related Colitis Induced by High-Fat Diet in Mice through Anti-Inflammatory Pathways

Ulcerative colitis is an inflammatory bowel disease characterized by inflammation in the mucosal and submucosal layers of the colon. Obesity is closely related to the occurrence and progression of colitis. The most plausible mechanism linking obesity and colitis is an excessive adipogenesis-related...

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Autores principales: Kwon, Hyung Jun, Chun, So Young, Lee, Eun Hye, Yoon, BoHyun, Han, Man-Hoon, Chung, Jae-Wook, Ha, Yun-Sok, Lee, Jun Nyung, Kim, Hyun Tae, Kim, Dae Hwan, Kwon, Tae Gyun, Kim, Bum Soo, Lee, Syng-Ook, Jang, Byung Ik
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10418620/
https://www.ncbi.nlm.nih.gov/pubmed/37569708
http://dx.doi.org/10.3390/ijms241512333
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author Kwon, Hyung Jun
Chun, So Young
Lee, Eun Hye
Yoon, BoHyun
Han, Man-Hoon
Chung, Jae-Wook
Ha, Yun-Sok
Lee, Jun Nyung
Kim, Hyun Tae
Kim, Dae Hwan
Kwon, Tae Gyun
Kim, Bum Soo
Lee, Syng-Ook
Jang, Byung Ik
author_facet Kwon, Hyung Jun
Chun, So Young
Lee, Eun Hye
Yoon, BoHyun
Han, Man-Hoon
Chung, Jae-Wook
Ha, Yun-Sok
Lee, Jun Nyung
Kim, Hyun Tae
Kim, Dae Hwan
Kwon, Tae Gyun
Kim, Bum Soo
Lee, Syng-Ook
Jang, Byung Ik
author_sort Kwon, Hyung Jun
collection PubMed
description Ulcerative colitis is an inflammatory bowel disease characterized by inflammation in the mucosal and submucosal layers of the colon. Obesity is closely related to the occurrence and progression of colitis. The most plausible mechanism linking obesity and colitis is an excessive adipogenesis-related inflammatory response, which causes mucosal dysfunction. Obesity and colitis are linked by several etiologic mechanisms, including excessive adipogenesis, lipotoxicity, pro-inflammatory adipokines/cytokines, macrophage polarization, oxidative stress, endoplasmic reticulum (ER) stress, and gut microbiota. These low-grade enteric inflammations cause mucosal layer damage, especially goblet cell dysfunction through mucin 2 (MUC2) misfolding, ultimately leading to colitis. Inhibiting the inflammatory response can be the most effective approach for treating obesity-related colitis. We focused on the anti-inflammatory effects of polyphenols in Protaectia brevitas larvae. The P. brevitas was prepared as a low molecular protein hydrolysate (PHPB) to increase the concentration of anti-inflammatory molecules. In the current study, we investigated the anti-inflammatory effect of PHPB in an obesity-induced colitis mouse model. Compared with the high-fat diet (HFD) group, the group treated with PHPB exhibited reduced body/organ/fat weight, appetite/food intake inhibition, hypolipidemic effect on ectopic fat, and anti-adipogenic mechanism through the AMPK signaling pathway. Furthermore, we observed attenuated expression of PPARγ and C/EBPα, inhibition of pro-inflammatory molecules, stimulation of anti-inflammatory molecules, probiotic-like effect against obesogenic gut microbiota, inhibition of macrophage polarization into M1, suppression of oxidative/ER stress, and reduction of Muc2 protein misfolding in colon. These diverse anti-inflammatory responses caused histological and functional recovery of goblet cells, eventually improving colitis. Therefore, our findings suggest that the protein hydrolysate of Protaetia brevitarsis can improve obesity-related colitis through its anti-inflammatory activities.
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spelling pubmed-104186202023-08-12 Protaetia Brevitarsis-Derived Protein Hydrolysate Reduces Obesity-Related Colitis Induced by High-Fat Diet in Mice through Anti-Inflammatory Pathways Kwon, Hyung Jun Chun, So Young Lee, Eun Hye Yoon, BoHyun Han, Man-Hoon Chung, Jae-Wook Ha, Yun-Sok Lee, Jun Nyung Kim, Hyun Tae Kim, Dae Hwan Kwon, Tae Gyun Kim, Bum Soo Lee, Syng-Ook Jang, Byung Ik Int J Mol Sci Article Ulcerative colitis is an inflammatory bowel disease characterized by inflammation in the mucosal and submucosal layers of the colon. Obesity is closely related to the occurrence and progression of colitis. The most plausible mechanism linking obesity and colitis is an excessive adipogenesis-related inflammatory response, which causes mucosal dysfunction. Obesity and colitis are linked by several etiologic mechanisms, including excessive adipogenesis, lipotoxicity, pro-inflammatory adipokines/cytokines, macrophage polarization, oxidative stress, endoplasmic reticulum (ER) stress, and gut microbiota. These low-grade enteric inflammations cause mucosal layer damage, especially goblet cell dysfunction through mucin 2 (MUC2) misfolding, ultimately leading to colitis. Inhibiting the inflammatory response can be the most effective approach for treating obesity-related colitis. We focused on the anti-inflammatory effects of polyphenols in Protaectia brevitas larvae. The P. brevitas was prepared as a low molecular protein hydrolysate (PHPB) to increase the concentration of anti-inflammatory molecules. In the current study, we investigated the anti-inflammatory effect of PHPB in an obesity-induced colitis mouse model. Compared with the high-fat diet (HFD) group, the group treated with PHPB exhibited reduced body/organ/fat weight, appetite/food intake inhibition, hypolipidemic effect on ectopic fat, and anti-adipogenic mechanism through the AMPK signaling pathway. Furthermore, we observed attenuated expression of PPARγ and C/EBPα, inhibition of pro-inflammatory molecules, stimulation of anti-inflammatory molecules, probiotic-like effect against obesogenic gut microbiota, inhibition of macrophage polarization into M1, suppression of oxidative/ER stress, and reduction of Muc2 protein misfolding in colon. These diverse anti-inflammatory responses caused histological and functional recovery of goblet cells, eventually improving colitis. Therefore, our findings suggest that the protein hydrolysate of Protaetia brevitarsis can improve obesity-related colitis through its anti-inflammatory activities. MDPI 2023-08-02 /pmc/articles/PMC10418620/ /pubmed/37569708 http://dx.doi.org/10.3390/ijms241512333 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Kwon, Hyung Jun
Chun, So Young
Lee, Eun Hye
Yoon, BoHyun
Han, Man-Hoon
Chung, Jae-Wook
Ha, Yun-Sok
Lee, Jun Nyung
Kim, Hyun Tae
Kim, Dae Hwan
Kwon, Tae Gyun
Kim, Bum Soo
Lee, Syng-Ook
Jang, Byung Ik
Protaetia Brevitarsis-Derived Protein Hydrolysate Reduces Obesity-Related Colitis Induced by High-Fat Diet in Mice through Anti-Inflammatory Pathways
title Protaetia Brevitarsis-Derived Protein Hydrolysate Reduces Obesity-Related Colitis Induced by High-Fat Diet in Mice through Anti-Inflammatory Pathways
title_full Protaetia Brevitarsis-Derived Protein Hydrolysate Reduces Obesity-Related Colitis Induced by High-Fat Diet in Mice through Anti-Inflammatory Pathways
title_fullStr Protaetia Brevitarsis-Derived Protein Hydrolysate Reduces Obesity-Related Colitis Induced by High-Fat Diet in Mice through Anti-Inflammatory Pathways
title_full_unstemmed Protaetia Brevitarsis-Derived Protein Hydrolysate Reduces Obesity-Related Colitis Induced by High-Fat Diet in Mice through Anti-Inflammatory Pathways
title_short Protaetia Brevitarsis-Derived Protein Hydrolysate Reduces Obesity-Related Colitis Induced by High-Fat Diet in Mice through Anti-Inflammatory Pathways
title_sort protaetia brevitarsis-derived protein hydrolysate reduces obesity-related colitis induced by high-fat diet in mice through anti-inflammatory pathways
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10418620/
https://www.ncbi.nlm.nih.gov/pubmed/37569708
http://dx.doi.org/10.3390/ijms241512333
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