Role of placental lactogens in regulating pancreatic beta-cell mass and function

胰岛含有合成胰岛素的？细胞，胰岛素是一种负责维持正常血糖的激素。我们知道，肌细胞的质量和功能是动态的，它可以通过增加肌细胞质量和胰岛素分泌来适应压力，比如怀孕。我们致力于研究？细胞如何对其环境作出反应，以及调节？细胞质量和功能的机制。此前，我们的研究发现，PRLR杂合性缺失的小鼠，即PrLR+/-小鼠，在妊娠期比野生型小鼠有更少的？细胞数量和更少的胰岛素分泌，这表明作用于PrLR的胎盘催乳素(Pls)对？细胞有生物学效应。由于PrlR的缺失发生在全身，而不是胰腺特有的，因此可能该表型是次要的，而不是整个Prlr介导的效应减弱。为了确定在怀孕期间调节？细胞适应的机制，我试图发现PERS如何调节？细胞质量和功能的机制。我们的总体假设是，在适应妊娠的过程中，PERS通过其受体(即Prlr)直接作用于？细胞，刺激其增殖、胰岛素合成和分泌。

Pancreatic islets contain ß cells that synthesize insulin, the hormone responsible for maintaining normal blood glucose. We know that ß-cell mass and function is dynamic, and it can adapt to stresses such as pregnancy by increasing ß-cell mass and insulin secretion. We endeavor to study how ß-cell responds to its environment and mechanisms that regulate ß-cell mass and function. Previously, our studies have found that mice with a heterozygous deletion of prolactin receptor (Prlr), i.e. the Prlr+/- mice, had lower ß-cell number and secreted less insulin than wild type mice during pregnancy, suggesting that placental lactogens (PLs), which act on Prlr, have biological effects on ß cells. Since the Prlr deletion is in the whole body, not pancreas-specific, it is possible that the phenotype is secondary to overall diminished Prlr-mediated effects. To determine the mechanisms mediating ß-cell adaptation during pregnancy, I am seeking to discover the mechanism of how PLs regulate ß-cell mass and function. Our overall hypothesis is that PLs act directly on ß cells through its receptor (i.e. Prlr) to stimulate proliferation, insulin synthesis and secretion in adaptation to pregnancy.