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Fig. 3 | Diabetology & Metabolic Syndrome

Fig. 3

From: Clinical aspects of pancreatogenic diabetes secondary to hereditary pancreatitis

Fig. 3

Schematic mechanism underling mutations-associated pancreatitis. The PRSS1 (Cationic Trypsinogen) mutation leads to a gain-of-function with an increased conversion of intrapancreatic trypsinogen to trypsin. The SPINK1 (Serine Protease Inhibitor Kazal type 1) and CTRC (Chymotrypsin C) mutations lead to loss of defenses against the activation of trypsinogen. Mutations in CPA1 (carboxypeptidase A1) generate misfolded proteins leading to endoplasmic reticulum stress

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