Title of project

PROLONG – PROtective genes in diabetic complications and LONGevity

Abstract

By 2050, diabetes is anticipated to affect 1.31 billion individuals. Numerous reports have recently highlighted alarming increase in the incidence of both type 1 and type 2 diabetes following COVID-19 infection across all ethnic groups. Despite this major burden, there is still no full understanding of diabetes heterogeneity and current classification fails to predict disease progression. Connecting patients’ electronic health records and drug registries with different genetic and other omics databases could improve the classification and predict complications outcome. To achieve this goal, we have begun to unmask mechanisms related to protection from vascular damage in patients with long-standing type 1 diabetes. These findings pointed to a potential beneficial shunting of glycolytic substrates towards the pentose phosphate and one carbon metabolism pathways to promote nucleotide biosynthesis in the liver. These processes seem to be linked to higher insulin sensitivity and lower liver fat content. Our recent transcriptomics data suggest that above mentioned processes have the key interlinked underlying mechanisms which are rooted in DNA repair and inflammation-related pathways. As a next step mechanistic and prospective studies investigating the diagnostic and prognostic significance of these findings as potential biomarkers for prevention of progression to complications should be performed.