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Cortisol is released in response to prolonged stresses; one situation when cortisol is released is when blood glucose level is low. In this situation cortisol acts on adipose tissue promoting fatty acid mobilization, and also promotes gluconeogenesis by degrading muscle proteins and converting them into pyruvate. Cortisol also stimulates gluconeogenesis by increasing the expression of PEP Carboxykinase the enzyme of gluconeogenensis pathway promoting the TCA Cycle intermediates or Oxaloacetate to convert into Phosphoenolpyruvate and promoting gluconeogenesis to balance the blood glucose level.

These are the same effects produced by glucagon to increase the blood glucose level when it is low.

My question then is what is the need for release of Cortisol? Also, if its release is important to control other pathways I haven't mentioned here, then why does cortisol produce the same effects as glucagon? Why is glucagon alone not enough to maintain blood glucose level?

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Since the ability to utilize glucose for energy is necessary for life (look at the effect of hypoglycemia on brain function, for example), it makes sense that the regulation of serum glucose concentration would have a number of pathways, that is, redundancy helps to ensure continued proper function should one of the regulatory mechanisms fail.

Glucagon is considered the main physiological response to hypoglycemia; however, epinephrine, growth hormone, and cortisol - in that order - and very probably other factors yet to be named/elucidated also help to increase plasma glucose when it drops.

This kind of redundancy is very common. Cortisol, epinephrine and growth hormone all have other effects on tissue unrelated to glucose as well.

Glucose Counterregulatory Responses to Hypoglycemia

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