Project Details
Abstract English
In 2019, diabetes was the direct cause of 1.5 million deaths and 48% of all deaths due to diabetes (Steinmetz et al., 2021). There is an ongoing need to further understand the pathophysiology and genetic distinct entities in this costly disease in order to prevent its occurrence. Even though T1D and T2D share common etiological features (e.g., apoptosis of pancreatic islet beta cells) and result in insulin deficiency, there might be some overlap in the pathogenesis of both T1D and T2D, but whether this is due to environmental, genetic, or biological pathway intersections, these effects remain to be determined. Additionally, evidence shows that the microbiota composition contributes to the proper functioning of human organisms, and they create a dynamic ecosystem that is modulated by internal and external factors (Aw and Fukuda, 2018). Altered composition of oral and gut bacteria can participate in the pathogenesis of diabetes (Bielka et al., 2022). Thus, it is of great importance to discover whether the oral/gut bacteria contribute to the development of these diseases of civilization. Understanding these factors can not only help to modify their course or to delay the appearance of complications, but also to prevent the onset of the disorders. The research aims to identify host-microbial signatures that will provide novel markers for predicting T1 and T2 Diabetes. We will define certain parameters based on the abundances of selected bacterial species, cytokines, and immunoglobulins. This result could strengthen our hypothesis of a potential protective role of the specific oral microbiome indiabetic individuals, and this could potentially help in patient management or therapeutic development implications.
Status | Finished |
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Effective start/end date | 1/02/23 → 1/02/24 |
Collaborative partners
- Dasman Diabetes Institute
- Ministry of Health
- Harvard School of Dental Medicine
- Tufts University
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