Please use this identifier to cite or link to this item:
|Title:||Insights into Transcriptional Regulation of Hepatic Glucose Production|
|Keywords:||Biochemistry, Genetics and Molecular Biology|
|Citation:||International Review of Cell and Molecular Biology. Vol.318, (2015), 203-253|
|Abstract:||© 2015 Elsevier Inc. Maintenance of systemic glucose homeostasis is pivotal in animals because most tissues, especially brain and red blood cells, rely on glucose as the sole energy source. The liver protects the body from hypoglycemia because it possesses two biochemical pathways, namely gluconeogenesis and glycogenolysis which provide glucose during starvation period. Posttranslational regulation by allosteric effectors and/or reversible phosphorylation of the key enzymes involved in these two pathways provide the rapid response for the immediate increase in the enzyme activities to accelerate rates of gluconeogenesis and glycogenolysis, but these mechanisms are insufficient for long-term control. Glucoregulatory hormones can alter the rate of enzyme synthesis at the transcriptional step by modulating the key transcription factors and coactivators, such as CREB/CRTC2, FoxO1, nuclear receptors, C/EBPα, hepatocyte nuclear factors, PGC1α, and CLOCK genes. Precise and well-coordinated regulation of activities of these transcription factors at the right time enables liver to synthesize or suppress glucose production, thus maintaining the proper function of tissues and organs during starvation and feeding cycles. Loss of function mutation or deregulation of these key transcription factors and coactivators can result in the pathophysiological condition, such as type 2 diabetes.|
|Appears in Collections:||Scopus 2011-2015|
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.