Cortisol & Weight gain?

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cortisol is the SUGAR hormone. it drives muscle protein breakdown for gluconeogenesis. if you have Cushing's, you are hyperglycemic, so pancreas is always secreting insulin, which tells fat cells to insert GLUT4 and make more fat. Your peripheral muscles waste away and you get trunchal obesity instead.

So it's your second guess.
 
cortisol is the SUGAR hormone. it drives muscle protein breakdown for gluconeogenesis. if you have Cushing's, you are hyperglycemic, so pancreas is always secreting insulin, which tells fat cells to insert GLUT4 and make more fat. Your peripheral muscles waste away and you get trunchal obesity instead.

So it's your second guess.


Thanks 🙂 So from what I understand it is more about the redistribution of fat --> break down of protein/fat to make sugar in some areas, and the deposition of the fat to form fat pads in other areas?
 
Thanks 🙂 So from what I understand it is more about the redistribution of fat --> break down of protein/fat to make sugar in some areas, and the deposition of the fat to form fat pads in other areas?

i wouldn't say fat redistribution, no. think back to your biochemistry. The gluconeogenic pathway is protein-> amino acids-> carbon skeletons/citric acid cycle intermediates/pyruvate-> malate-> glucose. Fat, by contrast, doesn't break down to glucose precursors, it breaks down to acetyl-CoA. You can use acetyl-CoA to make ketones, but not glucose; for that you need the citric acid cycle intermediates.

Cortisol doesn't have any lipolysis activity. If you have Cushing's, you have too much cortisol, which means you are breaking down protein (mostly muscles, and mostly in the periphery) and liver is making that protein into glucose that your body doesn't really need. Then the excess glucose gets made into fat in adipose cells because insulin is being secreted in response to hyperglycemia. So you have peripheral muscle being made into trunchal fat, hence the classic Cushingoid appearance with thin limbs and central obesity.
 
i wouldn't say fat redistribution, no. think back to your biochemistry. The gluconeogenic pathway is protein-> amino acids-> carbon skeletons/citric acid cycle intermediates/pyruvate-> malate-> glucose. Fat, by contrast, doesn't break down to glucose precursors, it breaks down to acetyl-CoA. You can use acetyl-CoA to make ketones, but not glucose; for that you need the citric acid cycle intermediates.

Cortisol doesn't have any lipolysis activity. If you have Cushing's, you have too much cortisol, which means you are breaking down protein (mostly muscles, and mostly in the periphery) and liver is making that protein into glucose that your body doesn't really need. Then the excess glucose gets made into fat in adipose cells because insulin is being secreted in response to hyperglycemia. So you have peripheral muscle being made into trunchal fat, hence the classic Cushingoid appearance with thin limbs and central obesity.

What you're saying makes sense save that BRS phys says that cortisol stimulates gluconeogenesis by increasing protein catabolism, decreasing glucose utilization and insulin sensitivity of adipose tissue and by increasing lipolysis (which provides more glycerol to the liver for gluconeogenesis).
 
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