RNA-seq of pancreatic islets from pregnant mice

ABSTRACT: During pregnancy, the energy requirements of the fetus impose changes in maternal metabolism. Increasing insulin resistance in the mother maintains nutrient flow to the growing fetus, while prolactin and placental lactogen counterbalance this resistance and prevent maternal hyperglycemia by driving expansion of the maternal population of insulin-producing beta-cells. However, the exact mechanisms by which the lactogenic hormones drive beta-cell expansion remain uncertain. Here we show that serotonin acts downstream of lactogen signaling to drive beta-cell proliferation. Serotonin synthetic enzyme Tph1 and serotonin production increased sharply in beta-cells during pregnancy or after treatment with lactogens in vitro. Inhibition of serotonin synthesis by dietary tryptophan restriction or Tp

INSTRUMENT(S): Illumina Genome Analyzer

ORGANISM(S): Mus musculus

SUBMITTER: Hail Kim 

PROVIDER: E-GEOD-21860 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress