Adrenergic regulation of lipolysis

JudoJosh

JudoJosh

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Following up from my last post on norephedrine (NE) mediated lipolysis where I explained how norephedrine (NE) interacts with a fat cell to contribute towards fat loss, this post will describe the role of both adrenoceptors play in regulating lipolysis. To quickly recap, catecholamines are the main regulatory hormones of lipid mobilization. The catecholamine NE binds to an adrenergic receptor on fat cells and this stimulates the breakdown of fatty acids so that they can be oxidized (burned).

There are two types of adrenoceptors in which the neurotransmitters can interact with. Each one playing a separate role in regulating the breakdown in cells. The two types are called alpha and beta adrenoreceptors. These are both present on the cell in various ratios depending on several various factors.

The binding of NE to the beta-receptors can be thought of as flipping the on switch on lipolysis. Remember the following cascade from the last post, NE -> adrenoceptor -> adenylate cyclase -> cAMP -> Protein Kinase A (PKA) -> Hormone Sensitive Lipase (HSL) -> lipolysis. Once the fatty acids have been separated from glycerol they are able to diffuse through the membrane of the adipose cell and enter into the bloodstream.

On the other hand, the a2-adrenoceptor can be conceptualized as an “off” switch for lipolysis. When NE is released from the vesicles & into the synaptic cleft it will either go and bind to a receptor on the cell or it will enter into the bloodstream. Some of the NE that enters the blood will end up being degraded by the enzymes monoamine oxidase and catechol-O-methyltransferase (COMT) while the rest of it is taken back up. This recycling of NE is mediated by the alpha-adrenoceptors and as a consequence, slows down the rate at which NE is being released.




Together both adrenoceptors work to regulate lipolysis. Activation of the beta-receptors increasing lipolysis and the a2-adrenoceptors acting in the feedback system inhibiting further stimulation of the beta-receptors.

In tissues where a2-adrenoceptors dominate over beta-receptors, the a2-adrenoceptors will have a lower threshold than the beta-receptors resulting in their activation first. During exercise, stimulation of the beta-receptors overpowers the inhibiting effect of the a2-adrenoceptors but at rest the a2-adrenoceptors dominate. Think of it as a dimmer switch with the intensity of the light representing the intensity of lipolysis. During exercise the lights in the room are fully on however at rest the lights become slightly dimmer but the room is still lit up but not as bright. This is because even in the absence of a agonist present, the a2-adrenoceptors will still slow down lipolysis. This gets made worse throughout our days with our daily lifestyle movement. Recall that a2-adrenoceptors have a lower threshold and outnumber the beta-receptors, so when there is a slight increase in NE, there will be an increased activation of the a2-adrenoceptors further decreasing lipolysis or continuing on with the dimmer switch analogy, making the room even darker. This make the a2-adrenoceptors the major lipolysis-regulating adrenoceptor and the target for many weight loss products. By blocking the activation of the a2-adrenoceptors we will get an increased neurotransmitter release thus increased lipolysis activity.
 
Driven2lift

Driven2lift

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thanks, I wasnt sure if anyone was actually reading these
Reading and subbed to all of them, educational contributions to AM are rarities and very much appreciated brother.
 

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