Need help in remembering metabolic pathways of cortisol vs. glucagon vs. insulin

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britesky89

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Hi, I'm having trouble remembering the different pathways of glucagon, cortisol, and insulin. It's hard to remember which one has gluconeogenesis, glycogenolysis, proteolysis, protein synthesis, lipolysis, lipid synthesis etc.

I've tried to just memorize the effects but that hasn't been working. I'm afraid I may be lacking understanding of the fundamentals of these hormone pathways.

Does anyone have a good explanation or easy way of differentiating and remembering the pathways?

Any help would be appreciated! There are so many confusing questions on step 1 where they ask which metabolites increase or decrease in various endocrine diseases.
 
Insulin drives the utilization and storage of ingested glucose. Glycogenesis, aerobic glycolysis, protein synthesis, and lipid synthesis.
Glucagon drives the mobilization of glucose in a low glucose environment (ie fasting). Glycogenolysis, proteolysis, and certain aspects of lipolysis.

Insulin and glucagon are antagonistic.

Cortisol is a bit strange. It's a stress hormone that has a synergistic effect with the catecholamines, so I think of cortisol as the hormone that puts the body on 'high alert' for future stress. Cortisol redistributes energy reserves such that your stored energy can be rapidly utilized once the appropriate catecholamine signalling begins. There is glycogenolysis (to increase availability of serum glucose), proteolysis, and a combination of lipogenesis/lipolysis. Lipogenesis occurs in the central areas (abdomen, trunk), and lipolysis occurs in the extremities-- think of where Cushingoid fat is distributed. Some other effects of cortisol include decreasing gluconeogenesis (gluconeogenesis consumes energy) and to increase cellular glucose uptake.

One oddball enzyme that I can think of off the top of my head is hormone-sensitive lipase, which increases the serum concentration of triglycerides in the periphery. The reason that it's an oddball enzyme is because it is activated by a decrease in insulin rather than an increase in glucagon.
 
That's a really good explanation!

Though, there's one action of glucagon that doesn't fit into mobilization : gluconeogenesis.

About the hormone sensitive lipase, it's helps to breakdown TG in the adipose tissue so how does it increase serum TG?
 
That's a really good explanation!

Though, there's one action of glucagon that doesn't fit into mobilization : gluconeogenesis.

About the hormone sensitive lipase, it's helps to breakdown TG in the adipose tissue so how does it increase serum TG?
Gluconeogenic precursors include lactate, amino acids, and glycerol-- the raw components for gluconeogenesis are provided by the catabolic effects of glucagon. It really is an example of mobilization if you think about it, as the physiological response to glucagon involves taking these precursor molecules from the periphery and converting them into a more biodigestable form: glucose.

The role of hormone-sensitive lipase in metabolism is to mobilize stored triglycerides from the periphery (adipose tissue) to FFA. The FFA can either be consumed directly by certain tissues, or they can be transported to the liver and converted to ketone bodies. The transportation from adipose tissue to the liver increases the serum concentration of TG.
 
Cortisol is a bit strange. It's a stress hormone that has a synergistic effect with the catecholamines, so I think of cortisol as the hormone that puts the body on 'high alert' for future stress. Cortisol redistributes energy reserves such that your stored energy can be rapidly utilized once the appropriate catecholamine signalling begins. There is glycogenolysis (to increase availability of serum glucose), proteolysis, and a combination of lipogenesis/lipolysis. Lipogenesis occurs in the central areas (abdomen, trunk), and lipolysis occurs in the extremities-- think of where Cushingoid fat is distributed. Some other effects of cortisol include decreasing gluconeogenesis (gluconeogenesis consumes energy) and to increase cellular glucose uptake.

I'm a little confused. In first aid under the topic of "rate limiting enzymes of metabolic processes" it says that cortisol is a positive regulator of glycogen synthase (glycogenesis).

Is there a good explanation for this?
 
I'm a little confused. In first aid under the topic of "rate limiting enzymes of metabolic processes" it says that cortisol is a positive regulator of glycogen synthase (glycogenesis).

Is there a good explanation for this?
Cortisol being a chronic stress hormone prepares the body to deal with long term stress. So it causes lipolysis/protolysis and induces insulin resistance by decreasing glucose uptake in the periphery leading to hyperglcemia. It indirectly induces glycogenolysis via glucagon depending on the stage (fasting v/s non-fasting).
By inducing glycogenesis (when the glucose levels are high) it is storing the excess glucose as glycogen for epinephrine to breakdown in acute stages of stress (flight/fight response).
Think of it this way: In a time of crisis it's taking the money out from the bank (lipolysis/protolysis), decreases wasteful expenditure (insulin resistance), keeps the excess money stored (glycogenesis) in the wallet/mattress at home (liver) for rapid access (epinephrine) and increasing the cash-flow (glycogenolysis) on a as needed basis (glucagon).
HTH
 
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Think of it this way: In a time of crisis it's taking the money out from the bank (lipolysis/protolysis), decreases wasteful expenditure (insulin resistance), keeps the excess money stored (glycogenesis) in the wallet/mattress at home (liver) for rapid access (epinephrine) and increasing the cash-flow (glycogenolysis) on a as needed basis (glucagon).
HTH

I love that explanation!! THANKS A LOT!
 
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