Endocrine, and Thermogenic Effects

E promotes the production and release of glucose from the liver by two related mechanisms  

A direct stimulatory effect on hepatic glycogenolysis Pj) mediated by cAMP-dependent phosphorylation of phosphorylase. This effect is dependent on prior storage of glycogen in the liver therefore, both insulin and cortisol serve to condition the liver for this effect. 

A direct activation of gluconeogenesis in the liver P2) via cAMP-dependent phosphorylation of the key gluconeogenic enzymes. This effect requires prior induction and maintenance of enzyme concentrations by cortisol. 

These two glucose-generating actions of E on the liver are enhanced in an additive fashion by glucagon which, like E, depends on cAMP mediation and cortisol conditioning. The fact that neural NE simultaneously causes a fall in the insulin/glucagon ratio indicates that the sympathetic nervous system has a supportive role. 

Neural NE and plasma E are both stimulators of adipocyte lipolysis, an effect that is mediated by )8,- and 63-adrenergic receptors and involves cAMP-mediated phosphorylation of hormone-sensitive lipase (HSL). There are regional differences in 3-adrenergic receptor density (visceral fat has more than subcutaneous fat), which determines that catecholamine is physiologically important. Note that receptors are low-affinity receptors that require high concentrations of catecholamines. They respond better to neural stimulation because of the higher local concentration of NE at the fat tissue site. 

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