Gluconeogenesis hormones that control

Longer lasting control of mineral metabolism is achieved by steroid hormones elaborated by the adrenal cortex and by synthetic analogues. Besides their actions on gluconeogenesis, glycogen deposition, protein metabolism and sexual characteristics, the corticosteriods influence calcium metabolism and the control of water and electrolyte equilibria, so that profound changes accompany their administration. 

The glucocorticoid cortisol is secreted from the adrenal cortex as a stress response under the control of adrenocorticotropic hormone (ACTH, corticotropin) produced by the anterior pituitary. Cortisol promotes catabolism by inducing synthesis of specific proteins. Cortisol binds to a cytosolic cortisol receptor which then translocates to the nucleus and switches on the expression of specific genes, notably that for PEP carboxykinase (PEPCK). Cortisol-induced expression of the key gluconeogenesis enzyme PEPCK increases levels of the enzyme and hence increases gluconeogenesis and available blood glucose. The cAMP-and cortisol-mediated pathways for induction of PEPCK expression are further linked by CREB-dependent expression of a coactivator protein PGC-1 that promotes cortisol-dependent expression of PEPCK. 

As was the case with glycolysis and gluconeogenesis, it would be futile for the cell to carry out glycogen synthesis and degradation simultaneously. The results achieved by the action of one pathway would be imdone by the other. This problem is avoided by a series of hormonal controls that activate the enzymes of one pathway while inactivating the enzymes of the other pathway. 

Now that we know something about the effects of hormones in triggering responses within the cell, we can return to and expand on some earlier points about metabolic control. In Section 18.3, we discussed some points about control mechanisms in carbohydrate metabolism. We saw at that time how glycolysis and gluconeogenesis can be regulated and how glycogen synthesis and breakdown can respond to the body s needs. Phosphorylation and dephosphorylation of the appropriate enzymes played a large role there, and that whole scheme is subject to hormonal action. 

In summary we can say that insulin lowers cyclic AMP levels in adipose tissue and liver when the cyclic AMP has first been raised by various hormonal manipulations. This fall in cyclic AMP seems to account for several important actions of insxilin, in particular its action on lipolysis, glycogen synthetase and phosphorylase in adipose tissue, and on gluconeogenesis, glycogenolysis and potassium output by the liver. Glucose transport in adipose tissue does not seem to be controlled by the cyclic AMP level and we have no evidence that the action of insulin on muscle is mediated by cyclic AMP. 

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