Abstract
During pregnancy, maternal β 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 β cell development and promotes regeneration after partial β cell ablation. During embryogenesis, Ctgf is expressed in pancreatic ducts, vasculature, and β 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 β cell proliferation, while β cell proliferation in virgin Ctgf(LacZ/+) females is unaffected. Additionally, α-cell proliferation, β cell size, and GSIS were unaffected in Ctgf(LacZ/+) mice, suggesting that vascular-derived Ctgf has a specific role in islet compensation during pregnancy.