par Arroyo, Maria Nicol 
;Cnop, Miriam ;Green, Jonathan ;Igoillo Esteve, Mariana
Référence International journal of molecular sciences, 22, 2
Publication Publié, 2021-01-01
;Cnop, Miriam ;Green, Jonathan ;Igoillo Esteve, Mariana Référence International journal of molecular sciences, 22, 2
Publication Publié, 2021-01-01
Article révisé par les pairs
| Résumé : | The global rise in type 2 diabetes results from a combination of genetic predisposition with environmental assaults that negatively affect insulin action in peripheral tissues and impair pancreatic β-cell function and survival. Nongenetic heritability of metabolic traits may be an important contributor to the diabetes epidemic. Transfer RNAs (tRNAs) are noncoding RNA molecules that play a crucial role in protein synthesis. tRNAs also have noncanonical functions through which they control a variety of biological processes. Genetic and environmental effects on tRNAs have emerged as novel contributors to the pathogenesis of diabetes. Indeed, altered tRNA aminoacylation, modification, and fragmentation are associated with β-cell failure, obesity, and insulin resistance. Moreover, diet-induced tRNA fragments have been linked with intergenerational inheritance of metabolic traits. Here, we provide a comprehensive review of how perturbations in tRNA biology play a role in the pathogenesis of monogenic and type 2 diabetes. |
