On December 31, 2021, Shrivastava, Vipul; Lee, Megan; Lee, Daniel; Pretorius, Marle; Radford, Bethany; Makkar, Guneet; Huang, Carol published an article.SDS of cas: 2358-84-1 The title of the article was Beta cell adaptation to pregnancy requires prolactin action on both beta and non-beta cells. And the article contained the following:
Pancreatic islets adapt to insulin resistance of pregnancy by up regulating β-cell mass and increasing insulin secretion. Previously, using a transgenic mouse with global, heterozygous deletion of prolactin receptor (Prlr+/-), we found Prlr signaling is important for this adaptation. However, since Prlr is expressed in tissues outside of islets as well as within islets and prolactin signaling affects β-cell development, to understand β-cell-specific effect of prolactin signaling in pregnancy, we generated a transgenic mouse with an inducible conditional deletion of Prlr from β-cells. Here, we found that β-cell-specific Prlr reduction in adult mice led to elevated blood glucose, lowed β-cell mass and blunted in vivo glucose-stimulated insulin secretion during pregnancy. When we compared gene expression profile of islets from transgenic mice with global (Prlr+/-) vs. β-cell-specific Prlr reduction (βPrlR+/-), we found 95 differentially expressed gene, most of them down regulated in the Prlr+/- mice in comparison to the βPrlR+/- mice, and many of these genes regulate apoptosis, synaptic vesicle function and neuronal development. Importantly, we found that islets from pregnant Prlr+/- mice are more vulnerable to glucolipotoxicity-induced apoptosis than islets from pregnant βPrlR+/- mice. These observations suggest that down regulation of prolactin action during pregnancy in non-β-cells secondarily and neg. affect β-cell gene expression, and increased β-cell susceptibility to external insults. The experimental process involved the reaction of Oxybis(ethane-2,1-diyl) bis(2-methylacrylate)(cas: 2358-84-1).SDS of cas: 2358-84-1
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