Long-term ingestion of β-lactoglobulin-bound AGEs induces colonic inflammation by modulating RAGE (TLR4)/MYD88/NF-κB signaling pathway and gut microbiota in mice
Thermally processed foods are rich in advanced glycation end products (AGEs). Our study aimed to investigate the effects of long-term ingestion of β-lactoglobulin bound AGEs (β-LG AGEs) on the gut microenvironment and underlying mechanisms. BALB/c mice were orally administered with β-LG AGEs (60/120...
| Main Authors: | , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2023-08-01
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| Series: | Journal of Functional Foods |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S1756464623002906 |
| _version_ | 1827871789257064448 |
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| author | Aiying Shi Lu Dong Yuekun Wu Xiaoxia Liu Wanhua Li Jin Wang Xuemeng Ji Huan Lv Yan Zhang Shuo Wang |
| author_facet | Aiying Shi Lu Dong Yuekun Wu Xiaoxia Liu Wanhua Li Jin Wang Xuemeng Ji Huan Lv Yan Zhang Shuo Wang |
| author_sort | Aiying Shi |
| collection | DOAJ |
| description | Thermally processed foods are rich in advanced glycation end products (AGEs). Our study aimed to investigate the effects of long-term ingestion of β-lactoglobulin bound AGEs (β-LG AGEs) on the gut microenvironment and underlying mechanisms. BALB/c mice were orally administered with β-LG AGEs (60/120 mg/kg·bw) for 16 weeks. In this study, β-LG AGEs significantly induced oxidative stress and inflammation (TNF-α, IL-1β and IL-6), caused the lipid metabolism disorder, and led to the intestinal barrier dysfunction. Besides, the relative abundance of Lactobacillus, Odoribacter, and Parasutterella were increased by β-LG AGEs, which was positively correlated with the inflammation and epithelium barrier damage. Furthermore, β-LG AGEs were found to significantly decrease the content of short-chain fatty acids, such as acetic, propionic, butyric, and valeric acids, in feces, likely due to the impact of β-LG AGEs on the gut microbiota composition and structure. Additionally, β-LG AGEs were found to significantly downregulate the expression of colonic tight junction proteins, indicating their potential impact on intestinal barrier function. The potential molecular mechanism involved the RAGE/TLR4-mediated activation of NF-κB signaling pathway. These findings shed light on the harmful effects of food-borne β-LG AGEs on gut health. |
| first_indexed | 2024-03-12T16:15:51Z |
| format | Article |
| id | doaj.art-d3ac28aa578c43e4b61413cd1385e92b |
| institution | Directory Open Access Journal |
| issn | 1756-4646 |
| language | English |
| last_indexed | 2024-03-12T16:15:51Z |
| publishDate | 2023-08-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Journal of Functional Foods |
| spelling | doaj.art-d3ac28aa578c43e4b61413cd1385e92b2023-08-09T04:32:37ZengElsevierJournal of Functional Foods1756-46462023-08-01107105690Long-term ingestion of β-lactoglobulin-bound AGEs induces colonic inflammation by modulating RAGE (TLR4)/MYD88/NF-κB signaling pathway and gut microbiota in miceAiying Shi0Lu Dong1Yuekun Wu2Xiaoxia Liu3Wanhua Li4Jin Wang5Xuemeng Ji6Huan Lv7Yan Zhang8Shuo Wang9Tianjin Key Laboratory of Food Science and Health, School of Medicine, Nankai University, Tianjin 300071, ChinaTianjin Key Laboratory of Food Science and Health, School of Medicine, Nankai University, Tianjin 300071, ChinaTianjin Key Laboratory of Food Science and Health, School of Medicine, Nankai University, Tianjin 300071, ChinaTianjin Key Laboratory of Food Science and Health, School of Medicine, Nankai University, Tianjin 300071, ChinaTianjin Key Laboratory of Food Science and Health, School of Medicine, Nankai University, Tianjin 300071, ChinaTianjin Key Laboratory of Food Science and Health, School of Medicine, Nankai University, Tianjin 300071, ChinaTianjin Key Laboratory of Food Science and Health, School of Medicine, Nankai University, Tianjin 300071, ChinaTianjin Key Laboratory of Food Science and Health, School of Medicine, Nankai University, Tianjin 300071, ChinaCorresponding authors.; Tianjin Key Laboratory of Food Science and Health, School of Medicine, Nankai University, Tianjin 300071, ChinaCorresponding authors.; Tianjin Key Laboratory of Food Science and Health, School of Medicine, Nankai University, Tianjin 300071, ChinaThermally processed foods are rich in advanced glycation end products (AGEs). Our study aimed to investigate the effects of long-term ingestion of β-lactoglobulin bound AGEs (β-LG AGEs) on the gut microenvironment and underlying mechanisms. BALB/c mice were orally administered with β-LG AGEs (60/120 mg/kg·bw) for 16 weeks. In this study, β-LG AGEs significantly induced oxidative stress and inflammation (TNF-α, IL-1β and IL-6), caused the lipid metabolism disorder, and led to the intestinal barrier dysfunction. Besides, the relative abundance of Lactobacillus, Odoribacter, and Parasutterella were increased by β-LG AGEs, which was positively correlated with the inflammation and epithelium barrier damage. Furthermore, β-LG AGEs were found to significantly decrease the content of short-chain fatty acids, such as acetic, propionic, butyric, and valeric acids, in feces, likely due to the impact of β-LG AGEs on the gut microbiota composition and structure. Additionally, β-LG AGEs were found to significantly downregulate the expression of colonic tight junction proteins, indicating their potential impact on intestinal barrier function. The potential molecular mechanism involved the RAGE/TLR4-mediated activation of NF-κB signaling pathway. These findings shed light on the harmful effects of food-borne β-LG AGEs on gut health.http://www.sciencedirect.com/science/article/pii/S1756464623002906Advanced glycation end productsGut microbiotaLipopolysaccharideTight junction proteinShort chain fatty acidsThe receptor of advanced glycation end products (Toll-like receptor 4)/myeloid differentiation factor 88/ nuclear factor kappa-B signal pathway |
| spellingShingle | Aiying Shi Lu Dong Yuekun Wu Xiaoxia Liu Wanhua Li Jin Wang Xuemeng Ji Huan Lv Yan Zhang Shuo Wang Long-term ingestion of β-lactoglobulin-bound AGEs induces colonic inflammation by modulating RAGE (TLR4)/MYD88/NF-κB signaling pathway and gut microbiota in mice Journal of Functional Foods Advanced glycation end products Gut microbiota Lipopolysaccharide Tight junction protein Short chain fatty acids The receptor of advanced glycation end products (Toll-like receptor 4)/myeloid differentiation factor 88/ nuclear factor kappa-B signal pathway |
| title | Long-term ingestion of β-lactoglobulin-bound AGEs induces colonic inflammation by modulating RAGE (TLR4)/MYD88/NF-κB signaling pathway and gut microbiota in mice |
| title_full | Long-term ingestion of β-lactoglobulin-bound AGEs induces colonic inflammation by modulating RAGE (TLR4)/MYD88/NF-κB signaling pathway and gut microbiota in mice |
| title_fullStr | Long-term ingestion of β-lactoglobulin-bound AGEs induces colonic inflammation by modulating RAGE (TLR4)/MYD88/NF-κB signaling pathway and gut microbiota in mice |
| title_full_unstemmed | Long-term ingestion of β-lactoglobulin-bound AGEs induces colonic inflammation by modulating RAGE (TLR4)/MYD88/NF-κB signaling pathway and gut microbiota in mice |
| title_short | Long-term ingestion of β-lactoglobulin-bound AGEs induces colonic inflammation by modulating RAGE (TLR4)/MYD88/NF-κB signaling pathway and gut microbiota in mice |
| title_sort | long term ingestion of β lactoglobulin bound ages induces colonic inflammation by modulating rage tlr4 myd88 nf κb signaling pathway and gut microbiota in mice |
| topic | Advanced glycation end products Gut microbiota Lipopolysaccharide Tight junction protein Short chain fatty acids The receptor of advanced glycation end products (Toll-like receptor 4)/myeloid differentiation factor 88/ nuclear factor kappa-B signal pathway |
| url | http://www.sciencedirect.com/science/article/pii/S1756464623002906 |
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