Fig. 4

Role of eIF5A in normal and pathologic development of pancreas. Genetic deletion (upper panel). Developmental impact of Dhps and eIF5A knock-out specifically in pancreas of mice (from Padgett et al. [129]). Inducible knock-out of Dhps in pancreatic beta cells following by high fat diet inducing hyperglycemia (from Levasseur et al. [72]). Pharmacological inhibition (lower panel). Impact of GC7 treatment (DHPS inhibitor) on pathological features of Type 1 (streptozotocin “STZ” treatment, from Maier et al. [48]) or Type 2 diabetes (db/db mice mutated for Leptin receptor, from Robbins et al. [76]) mouse models. Impact of GC7 treatment on humanized (antigen presenting cells expressing hMHCII) transgenic mice for hGAD65 (glutamic acid decarboxylase) immunized with adenoviral vectors carrying GAD65, leading to auto-immune response against beta cells and ultimately to Type 1 diabetes induction (from Imam et al. [75])