Advanced Glycation End Products and Inflammation in Type 1 Diabetes Development
Type 1 diabetes (T1D) is an autoimmune disease in which the β-cells of the pancreas are attacked by the host’s immune system, ultimately resulting in hyperglycemia. It is a complex multifactorial disease postulated to result from a combination of genetic and environmental factors. In parallel with i...
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| Format: | Article |
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MDPI AG
2022-11-01
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| Series: | Cells |
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| Online Access: | https://www.mdpi.com/2073-4409/11/21/3503 |
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| author | Chenping Du Rani O. Whiddett Irina Buckle Chen Chen Josephine M. Forbes Amelia K. Fotheringham |
| author_facet | Chenping Du Rani O. Whiddett Irina Buckle Chen Chen Josephine M. Forbes Amelia K. Fotheringham |
| author_sort | Chenping Du |
| collection | DOAJ |
| description | Type 1 diabetes (T1D) is an autoimmune disease in which the β-cells of the pancreas are attacked by the host’s immune system, ultimately resulting in hyperglycemia. It is a complex multifactorial disease postulated to result from a combination of genetic and environmental factors. In parallel with increasing prevalence of T1D in genetically stable populations, highlighting an environmental component, consumption of advanced glycation end products (AGEs) commonly found in in Western diets has increased significantly over the past decades. AGEs can bind to cell surface receptors including the receptor for advanced glycation end products (RAGE). RAGE has proinflammatory roles including in host–pathogen defense, thereby influencing immune cell behavior and can activate and cause proliferation of immune cells such as islet infiltrating CD8<sup>+</sup> and CD4<sup>+</sup> T cells and suppress the activity of T regulatory cells, contributing to β-cell injury and hyperglycemia. Insights from studies of individuals at risk of T1D have demonstrated that progression to symptomatic onset and diagnosis can vary, ranging from months to years, providing a window of opportunity for prevention strategies. Interaction between AGEs and RAGE is believed to be a major environmental risk factor for T1D and targeting the AGE-RAGE axis may act as a potential therapeutic strategy for T1D prevention. |
| first_indexed | 2024-03-09T19:11:42Z |
| format | Article |
| id | doaj.art-cdf0b8a49dd24772ad56c2ca4bebc576 |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-09T19:11:42Z |
| publishDate | 2022-11-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cells |
| spelling | doaj.art-cdf0b8a49dd24772ad56c2ca4bebc5762023-11-24T04:09:50ZengMDPI AGCells2073-44092022-11-011121350310.3390/cells11213503Advanced Glycation End Products and Inflammation in Type 1 Diabetes DevelopmentChenping Du0Rani O. Whiddett1Irina Buckle2Chen Chen3Josephine M. Forbes4Amelia K. Fotheringham5Glycation and Diabetes Complications Group, Mater Research Institute-The University of Queensland, Translational Research Institute, Woolloongabba 4102, AustraliaGlycation and Diabetes Complications Group, Mater Research Institute-The University of Queensland, Translational Research Institute, Woolloongabba 4102, AustraliaGlycation and Diabetes Complications Group, Mater Research Institute-The University of Queensland, Translational Research Institute, Woolloongabba 4102, AustraliaSchool of Biomedical Sciences, Faculty of Medicine, The University of Queensland, St Lucia 4072, AustraliaGlycation and Diabetes Complications Group, Mater Research Institute-The University of Queensland, Translational Research Institute, Woolloongabba 4102, AustraliaGlycation and Diabetes Complications Group, Mater Research Institute-The University of Queensland, Translational Research Institute, Woolloongabba 4102, AustraliaType 1 diabetes (T1D) is an autoimmune disease in which the β-cells of the pancreas are attacked by the host’s immune system, ultimately resulting in hyperglycemia. It is a complex multifactorial disease postulated to result from a combination of genetic and environmental factors. In parallel with increasing prevalence of T1D in genetically stable populations, highlighting an environmental component, consumption of advanced glycation end products (AGEs) commonly found in in Western diets has increased significantly over the past decades. AGEs can bind to cell surface receptors including the receptor for advanced glycation end products (RAGE). RAGE has proinflammatory roles including in host–pathogen defense, thereby influencing immune cell behavior and can activate and cause proliferation of immune cells such as islet infiltrating CD8<sup>+</sup> and CD4<sup>+</sup> T cells and suppress the activity of T regulatory cells, contributing to β-cell injury and hyperglycemia. Insights from studies of individuals at risk of T1D have demonstrated that progression to symptomatic onset and diagnosis can vary, ranging from months to years, providing a window of opportunity for prevention strategies. Interaction between AGEs and RAGE is believed to be a major environmental risk factor for T1D and targeting the AGE-RAGE axis may act as a potential therapeutic strategy for T1D prevention.https://www.mdpi.com/2073-4409/11/21/3503type 1 diabetesdietary AGEsRAGEautoimmunity |
| spellingShingle | Chenping Du Rani O. Whiddett Irina Buckle Chen Chen Josephine M. Forbes Amelia K. Fotheringham Advanced Glycation End Products and Inflammation in Type 1 Diabetes Development Cells type 1 diabetes dietary AGEs RAGE autoimmunity |
| title | Advanced Glycation End Products and Inflammation in Type 1 Diabetes Development |
| title_full | Advanced Glycation End Products and Inflammation in Type 1 Diabetes Development |
| title_fullStr | Advanced Glycation End Products and Inflammation in Type 1 Diabetes Development |
| title_full_unstemmed | Advanced Glycation End Products and Inflammation in Type 1 Diabetes Development |
| title_short | Advanced Glycation End Products and Inflammation in Type 1 Diabetes Development |
| title_sort | advanced glycation end products and inflammation in type 1 diabetes development |
| topic | type 1 diabetes dietary AGEs RAGE autoimmunity |
| url | https://www.mdpi.com/2073-4409/11/21/3503 |
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