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

Author:

Kwon Hyung Jun1,Chun So Young2ORCID,Lee Eun Hye3,Yoon BoHyun3,Han Man-Hoon4ORCID,Chung Jae-Wook5ORCID,Ha Yun-Sok5ORCID,Lee Jun Nyung5,Kim Hyun Tae5ORCID,Kim Dae Hwan6,Kwon Tae Gyun5,Kim Bum Soo5ORCID,Lee Syng-Ook7ORCID,Jang Byung Ik8

Affiliation:

1. Department of Surgery, School of Medicine, Kyungpook National University, Daegu 41566, Republic of Korea

2. BioMedical Research Institute, Kyungpook National University Hospital, Daegu 41944, Republic of Korea

3. Joint Institute for Regenerative Medicine, Kyungpook National University, Daegu 41566, Republic of Korea

4. Department of Pathology, School of Medicine, Kyungpook National University, Daegu 41566, Republic of Korea

5. Department of Urology, School of Medicine, Kyungpook National University, Daegu 41566, Republic of Korea

6. Department of Laboratory Animal Research Support Team, Yeungnam University Medical Center, Daegu 42415, Republic of Korea

7. Department of Food Science and Technology, Keimyung University, Daegu 42601, Republic of Korea

8. Department of Internal Medicine, School of Medicine, Yeungnam University, Daegu 42415, Republic of Korea

Abstract

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.

Funder

2021 Yeungnam University Research Grant

Publisher

MDPI AG

Subject

Inorganic Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Computer Science Applications,Spectroscopy,Molecular Biology,General Medicine,Catalysis

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