Fig. 7

Summary and schematic representation of the study hypothesis. HFHS-induced lipotoxicity (untreated NAFP) downregulated the expression of miR-1976 and thereby upregulated the expression of pancreatic DDX58, NFκB1, and CHUK mRNAs. Activating the cGAS-STING signaling pathway stimulated diverse downstream signaling pathways including promoting the expression of inflammatory and fibrotic responses (NFκB1, Caspase-3, and increase in area percentage of collagen fibers). On benzyl propylene glycoside treatment, increased expression of miR-1976 inhibited the expression of its target genes (DDX58, NFκB1, and CHUK). Inhibiting the cGAS-STING signaling pathway reversed pathological disturbances manifested by decreased inflammation and fibrosis observed in the untreated NAFP. HFHS: high fat and high sucrose diet, NAFP: non-alcoholic fatty pancreas