Gluconeogenesis cortisol

It is not possible, however, to separate the effects very clearly one cannot ascribe the glucocorticoid effect alone to one hormone and the mineralcorticoid effect alone to another. But within the range of physiological concentrations, aldosterone appears to regulate electrolyte balance, and cortisol, gluconeogenesis. 

Cortisol-induced lipolysis not only provides substrates for gluconeogenesis (formation of glucose from noncarbohydrate sources) but it also increases the amount of free fatty acids in the blood. As a result, the fatty acids are used by muscle as a source of energy and glucose is spared for the brain to use to form energy. 

Figure F -6. Cortisol and Glucagon Stimulate Gluconeogenesis Through Enhancer Mechanisms...

Cortisol regulates gluconeogenesis by activation of genes which express some gluconeogenic enzymes so that the concentration of these enzymes is increased. 

Hormones can modify the concentration of precursors, particularly the lipolytic hormones (growth hormone, glucagon, adrenaline) and cortisol. The lipolytic hormones stimulate lipolysis in adipose tissue so that they increase glycerol release and the glycerol is then available for gluconeogenesis. Cortisol increases protein degradation in muscle, which increases the release of amino acids (especially glutamine and alanine) from muscle (Chapter 18). 

In relatively recent years, it has become clear that under-nntrition of mother leads to low birth weight of the baby and this can increase the risk of development of degenerative disease in later life, e.g. hypertension, obesity, type 2 diabetes. One hypothesis is that the foetus adapts meta-bolically to deficiencies by increasing the number of cells in organs that perform specific functions that can overcome the deficiency, e.g. an increase in the number of liver cells that carry out gluconeogenesis, an increase in cells in the adrenal cortex to produce more of the chronic stress hormone, cortisol. These changes are carried over into adnlthood which can lead to an inadequate response of the liver to insulin so that insulin resistance develops. So far, however, it is unclear whether deficiencies in specific nntrients or undemutrition per se are responsible for snch changes (Chapter 15). 

Glucocorticoids—mainly cortisol (see p. 374)—induce all of the key enzymes involved in gluconeogenesis [4, 6, 8, 9]. At the same time, they also induce enzymes involved in amino acid degradation and thereby provide precursors for gluconeogenesis. Regulation of the expression of PEP carbo>Q -kinase, a key enzyme in gluconeogenesis, is discussed in detail on p. 244. 

Phosphoenolpyruvate carboxykinase (PEP-CK), a key enzyme in gluconeogenesis, is regulated by several hormones, all of which affect the transcription of the PEP-CK gene. Cortisol, glucagon, and thyroxin induce PEP-CK, while insulin inhibits its induction (see p. 158). 

The first example shows the circadian rhythm of the cortisol level. As an activator of gluconeogenesis (see p. 158), cortisol is mainly released in the early morning, when the liver s glycogen stores are declining. During the day, the plasma cortisol level declines. 

Individuals with chronic liver disease may have disorders of fluid and electrolyte balance, including ascites, edema, and effusions. Alterations of whole body potassium induced by vomiting and diarrhea, as well as severe secondary aldosteronism, may contribute to muscle weakness and can be worsened by diuretic therapy. The metabolic derangements caused by metabolism of large amounts of ethanol can result in hypoglycemia, as a result of impaired hepatic gluconeogenesis, and in ketosis, caused by excessive lipolytic factors, especially increased cortisol and growth hormone. 

Glucocorticoids Adrenal cortex Cortisol Promotes gluconeogenesis and glycogen formation enhances fat and protein degradation... 

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. 

Cortisol. Cortisol, secreted by the adrenal cortex in response to adrenocorticotropic hormone (ACTH), stimulates gluconeogenesis and increases the breakdown of protein and fat. Patients with Cushing s syndrome have increased cortisol owing to a tumor or hyperplasia of the adrenal cortex and may become hyperglycemic. In contrast, people with Addisons disease have adrenocortical insufficiency because of destruction or atrophy of the adrenal cortex and may exhibit hypoglycemia. ... 

Overactivity of gluconeogenesis due to increased secretion of catecholamines, cortisol, or growth hormone or an increase in the glucagon/insulin ratio (Chapter 22) leads to hyperglycemia and causes many metabolic problems. 

Cortisol, by inhibiting glucose utilization in peripheral tissues, exerts a mild antianabolic effect on these tissues this effect diminishes their rate of amino acid incorporation, thus making available more amino acids for metabolism by these tissues, but mainly for hepatic protein synthesis and gluconeogenesis. 

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