Gluconeogenesis glucagon

Glucagon is secreted as a response to hypoglycemia and activates both glycogenolysis and gluconeogenesis in the liver, causing release of glucose into the blood. 

In adipose tissue, the effect of the decrease in insulin and increase in glucagon results in inhibition of lipo-genesis, inactivation of lipoprotein lipase, and activation of hormone-sensitive lipase (Chapter 25). This leads to release of increased amounts of glycerol (a substrate for gluconeogenesis in the liver) and free fatty acids, which are used by skeletal muscle and liver as their preferred metabolic fuels, so sparing glucose. 

Gs Glucagon, 3-adrenergics T Adenylyl cyclase T Cardiac Ca +, CL, and Na+ channels Gluconeogenesis, lipolysis, glycogenolysis... 

Glucagon Gs-cAMP-A kinase glycogen breakdown (muscle), gluconeogenesis (liver)... 

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

Insulin and glucagon regulate gluconeogenesis via changes in cyclic AMP concentration. 

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). 

Insulin inhibits glycogenolysis and gluconeogenesis. Glucagon opposes the effects of insulin and therefore helps to maintain the blood glucose level so that it has the same end result as that of fatty acid oxidation (See Figure 12.14). 

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). 

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