Vascular-Derived Connective Tissue Growth Factor (Ctgf) Is Critical For Pregnancy-Induced Cell Hyperplasia In Adult Mice

During pregnancy, maternal cells undergo compensatory changes including hypertrophy, hyperplasia, and increased glucose-stimulated insulin secretion (GSIS). Failure of these adaptations to occur can result in gestational diabetes mellitus. The secreted protein, Connective tissue growth factor (Ctgf), is critical for normal cell development and promotes regeneration after partial cell ablation. During embryogenesis, Ctgf is expressed in pancreatic ducts, vasculature, and cells. In the adult pancreas, Ctgf is expressed only in the vasculature. Here, we report that pregnant mice with global Ctgf haploinsufficiency (Ctgf(LacZ/+)) have an impairment in maternal cell proliferation, while cell proliferation in virgin Ctgf(LacZ/+) females is unaffected. Additionally, -cell proliferation, cell size, and GSIS were unaffected in Ctgf(LacZ/+) mice, suggesting that vascular-derived Ctgf has a specific role in islet compensation during pregnancy.