Expression analysis of control and low protein fed mouse offspring subsequently treated with multiple low doses of STZ

Low protein (LP) during gestation leads to low birth weight and poor fetal growth, with altered islet development and glucose intolerance in adulthood. Additionally, LP offspring fail to regenerate their β-cells following depletion with streptozotocin (STZ), in contrast to control-fed offspring that are capable of β-cell regeneration. Our objective was to identify genes and signalling pathways that may be critically altered in LP offspring rendering them susceptible to develop long term glucose intolerance and decreased β-cell plasticity. Pregnant Balb/C mice were place on a control (20% protein) or isocaloric low protein (8%) diet for the period of gestation, and then all dams were switch to the control diet at birth. Female offspring were injected with streptozotocin (35 mg/kg body weight; sodium citrate buffer 0.1 mol/L, pH 4.5) or vehicle (sham). Total RNA was extracted from pancreas of 30 day old female offspring (n=3) and hybridized to Affymetrix GeneChips.