Jeung S. Yun

TL;DR: It is established that a modest (2-fold) increase in PEPCK gene expression in vivo is sufficient to increase HGP without affecting FFA concentrations, and that FFA and/or IRS-1 signaling plays an important role in downstream insulin signal transduction pathways involved in control of gluconeogenesis and progression to type II diabetes mellitus.

TL;DR: It is established that −460 bp of 5′-flanking sequence is sufficient to mediate the induction of PEPCK gene transcription in genetically obesedb/db mice during the development of hyperglycemia and that the mechanism underlying increased expression of gluconeogenic enzymes in thedb/db mouse requires the action of glucocorticoids.

TL;DR: Evidence is provided for the interaction of insulin and glucocorticoid regulatory elements in the control of PEPCK gene transcription and an important role of glucoc Corticoids as a gluconeogenic activator during diabetes is suggested.

TL;DR: Comparison of results with data obtained from matings of normal female mice to transgenic males from the same lines suggests that reduced fetal growth is due primarily to maternal genotype, while reduced "transmission" of the hybrid genes is not, and presumably reflects increased mortality of transgenic progeny at various stages of development.

TL;DR: It is concluded that infertility of transgenic female mice with hGH expression is due to activation of the TIDA system, suppression of endogenous PRL release, and luteal deficiency.