ORCID Profile
0000-0002-5851-0439
Current Organisation
University of Arizona
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Publisher: American Physiological Society
Date: 02-2008
DOI: 10.1152/AJPENDO.00639.2007
Abstract: Hepatic glucose production is normally activated at birth but has been observed in response to experimental hypoglycemia in fetal sheep. The cellular basis for this process remains unknown. We determined the impact of 2 wk of fetal hypoglycemia during late gestation on enzymes responsible for hepatic gluconeogenesis, focusing on the insulin-signaling pathway, transcription factors, and coactivators that regulate gluconeogenesis. Hepatic phospho enolpyruvate carboxykinase and glucose-6-phosphatase mRNA increased 12-fold and 7-fold, respectively, following chronic hypoglycemia with no change in hepatic glycogen. Chronic hypoglycemia decreased fetal plasma insulin with no change in glucagon but increased plasma cortisol 3.5-fold. Peroxisome proliferator-activated receptor-γ coactivator-1α mRNA and phosphorylation of cAMP response element binding protein at Ser 133 were both increased, with no change in Akt, forkhead transcription factor FoxO1, hepatocyte nuclear factor-4α, or CCAAT enhancer binding protein-β. These results demonstrate that chronic fetal hypoglycemia triggers signals that can activate gluconeogenesis in the fetal liver.
Publisher: Elsevier BV
Date: 2004
Publisher: MDPI AG
Date: 30-10-2023
Publisher: Wiley
Date: 13-03-2017
DOI: 10.1113/JP273555
Publisher: Cambridge University Press
Date: 04-05-2006
Publisher: Wiley
Date: 05-2005
No related grants have been discovered for Sean Limesand.