In the β-cell, the expression of phosphoglucomutase 1 (PGM1), a type 1 diabetes risk gene, is reduced by double-stranded RNA exposure, modeled by polyinosinic:polycytidylic acid transfection. Deficient PGM1 expression disrupts central carbon metabolism, protein glycosylation, and autophagic flux. These changes precipitate endoplasmic reticulum stress and mitochondrial dysfunction, potentially augmenting type 1 diabetes development.
Ye et al. (Tue,) studied this question.