BS Biochemical Pharmacology, State University of New York at Buffalo
Ph.D Cell Biology, University of Alabama at Birmingham
During pregnancy, the developing fetus creates an increased demand for insulin that requires compensatory actions to support maternal health. These adaptations are achieved as a result of beta cell expansion, improved sensitivity to glucose, and enhanced glucose stimulated insulin secretion within the maternal islets. Failure of these actions to occur results in gestational diabetes mellitus (GDM), a condition that occurs in 3-7% of pregnancies and is characterized by high maternal blood glucose levels and an increased risk of preeclampsia and C-sections, as well as increased risk for Type 2 diabetes later in life for both mother and fetus. Our data indicates that CTGF, a protein with known roles in embryonic beta cell proliferation, is re-expressed in maternal beta cells during pregnancy, and pregnant mice with haploinsufficiency of CTGF display impaired glucose tolerance, similar to GDM. Using mutant CTGF alleles, I aim determine what role CTGF plays in the increase in beta cell proliferation, improved sensitivity to glucose, and enhanced GSIS that occurs during pregnancy. Furthermore, CTGF has known effects on the TGF-beta, BMP, and Wnt signaling pathways. As such, I will use reporter mice as well as commercially available assays to determine if CTGF influences these pathways to mediate glucose clearance during pregnancy.