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. Author manuscript; available in PMC: 2017 Nov 7.
Published in final edited form as: Cell Metab. 2014 Dec 2;20(6):979–990. doi: 10.1016/j.cmet.2014.11.004

Figure 6. Model of hGH-Induced Phenotypic Changes in Pdx1-CreLate.

Figure 6

β Cells

Pdx1-promoter-driven expression of the hGH minigene causes biosynthesis and secretion of hGH, which exerts autocrine or paracrine effects after binding to PRLR on β cells. This causes STAT5 phosphorylation and pregnancy-like phenotypic changes, such as enhanced β cell mass and serotonin (5-HT) production. In addition, expression of the hGH minigene causes pregnancy-unrelated changes, such as reduction of GLUT2 expression and partial loss of glucose-induced insulin release. Lower GLUT2-mediated uptake and higher β cell mass protect against the diabetogenic effect of the β cell toxin STZ.