Journal of Comprehensible Results - Ria Shah

Costin BN, Dever SM, Miles MF (2013).
Ethanol Regulation of Serum Glucocorticoid
Kinase 1 Expression in DBA2/J Mouse Prefrontal Cortex
PLoS ONE 8:e72979.

(Translated by Ria Shah)

Abstract

The experiment was carried out to understand the biological process of ethanol consumption in the body. The hypothalamus pituitary adrenal (HPA) axis is known to release glucocorticoid hormones in response to stress caused by alcohol.

In a previous study, the gene serum glucocorticoid kinase 1 (sgk1) was selected for further analysis. Due to its function in intracellular signaling, regulating ion channels, cell growth, learning, and memory. It was hypothesized acute alcohol influences the activation glucocorticoid and transcription of glucocorticoid gene, sgk1.

To test this hypothesis several experiments were carried out to understand effect of acute and chronic alcohol, from the molecular to protein level of sgk1. The results from the experiment suggest acute ethanol causes an upregulation of sgk1 via glucocorticoid receptor binding to the sgk1 promotor region. The glucocorticoid receptor is activated by the release of corticosterone from the adrenal gland involved in HPA axis. Overall, acute and chronic ethanol dysregulates of HPA axis. Furthermore, a decrease in sgk1 protein and phosphorylation of sgk1 was seen after 15 minutes of ethanol consumption.