The physiologically relevant catecholamines are epinephrine (E), non-epinephrine (NE) and dopamine (DA). These catecholamines regulate fat metabolism (lipolysis). Adipose tissue cells (or adipocytes) possess beta-Adrenergic receptors, and in response to catecholamines of either sympathetic or adrenal origin, lipolysis stimulated.
Epinephrine- induced cAMP production activates a hormone sensitive lipase, triglyceride lipase which metabolizes fats into free fatty acids (FFAs) and glycerol. The FFAs released into the blood are then used directly by certain tissues (brain, cardiac muscles etc.) as source of energy or they may be used in liver in the formation of glucose.
Beta-adrenergic receptors- cAMP is the intracellular second messenger in the glycogenolytic response to beta adrenergic stimulation by epinephrine. Cellular responses to beta Adrenergic receptor stimulation are linked to adenylate cyclase activation and cAMP formation.
Although, both glucagon and epinephrine stimulate glycogenolysis, they do so through separate receptors linked to a common adenylate cyclase.
The beta adrenergic receptor also undergoes desensitization due to a rapid attenuation of the stimulated rate of cAMP generation.
Epinephrine- induced cAMP production activates a hormone sensitive lipase, triglyceride lipase which metabolizes fats into free fatty acids (FFAs) and glycerol. The FFAs released into the blood are then used directly by certain tissues (brain, cardiac muscles etc.) as source of energy or they may be used in liver in the formation of glucose.
Beta-adrenergic receptors- cAMP is the intracellular second messenger in the glycogenolytic response to beta adrenergic stimulation by epinephrine. Cellular responses to beta Adrenergic receptor stimulation are linked to adenylate cyclase activation and cAMP formation.
Although, both glucagon and epinephrine stimulate glycogenolysis, they do so through separate receptors linked to a common adenylate cyclase.
The beta adrenergic receptor also undergoes desensitization due to a rapid attenuation of the stimulated rate of cAMP generation.
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