PMC:3852299 / 30850-31944 JSONTXT

{"project":"2_test","denotations":[{"id":"24103554-15917397-70233243","span":{"begin":438,"end":441},"obj":"15917397"},{"id":"24103554-14507910-70233244","span":{"begin":915,"end":918},"obj":"14507910"},{"id":"24103554-9183567-70233245","span":{"begin":919,"end":922},"obj":"9183567"},{"id":"24103554-9091804-70233246","span":{"begin":984,"end":987},"obj":"9091804"},{"id":"24103554-11984591-70233247","span":{"begin":1089,"end":1092},"obj":"11984591"}],"text":"Physiological effects of cortisol\nCortisol stimulates gluconeogenesis and fatty-acid mobilisation in the liver and adipose tissue. One of the most important effects of cortisol is that it upregulates glucose production. In the liver, cortisol increases the expression of the gluconeogenic enzymes phosphoenolpyruvate carboxykinase-C (PEPCK-C) and glucose-6-phosphatase (G6Pase), which releases glucose from glycogen into the circulation [165]. Glucocorticoids primarily act by the activation of the glucocorticoid receptor (GR) and the regulation of transcription. The GR is a ligand-regulated nuclear receptor that belongs to the steroid hormone receptor family. The GRs are expressed in almost all tissues. Upon binding by cortisol, the GR moves to the nucleus, binds specific glucocorticoid response elements (GRE) and recruits co-activators and co-repressors, which can increase or decrease gene transcription [166,167]. The GR can also alter nuclear translation without the GRE [168] and cortisol can also exert non-genomic actions in stimulating endothelial nitric oxide production [169]."}