"Insulin and triiodothyronine (T3) increase the binding of LDL to liver cells, whereas glucocorticoids (e.g., dexamethasone, CORTISOL) have the opposite effect. The precise mechanism for these effects is unclear but may be mediated through the regulation of apoB degradation. The effects of insulin a…
"Insulin and triiodothyronine (T3) increase the binding of LDL to liver cells, whereas glucocorticoids (e.g., dexamethasone, CORTISOL) have the opposite effect. The precise mechanism for these effects is unclear but may be mediated through the regulation of apoB degradation. The effects of insulin and T3 on hepatic LDL binding may explain the hypercholesterolemia and increased risk of atherosclerosis that have been shown to be associated with uncontrolled diabetes or hypothyroidism"
So, reintroducing insulin in the context of low-carb i.e. low-insulin environment, the number of receptors in the liver increases. Look analoguous to glut4 reseptors being invited to cell surface by insulin.
This should go both ways, explaining the high-responders rise of ldl when going to keto.
I need to study up on this a bit. I guess. Sigh. Long ago I determined (to my own satisfaction, at least) that lipids don't play much, if any, role in heart disease and that the lipid hypothesis was incorrect. Since then, I have avoided spending much time reading about lipids, especially since there is so much other really interesting and important stuff to read about.
Hi, some additional info to oreo magic:
"Insulin and triiodothyronine (T3) increase the binding of LDL to liver cells, whereas glucocorticoids (e.g., dexamethasone, CORTISOL) have the opposite effect. The precise mechanism for these effects is unclear but may be mediated through the regulation of apoB degradation. The effects of insulin and T3 on hepatic LDL binding may explain the hypercholesterolemia and increased risk of atherosclerosis that have been shown to be associated with uncontrolled diabetes or hypothyroidism"
https://themedicalbiochemistrypage.org/lipoproteins-blood-lipids-and-lipoprotein-metabolism/#:~:text=Insulin%20and%C2%A0triiodothyronine,uncontrolled%20diabetes%20or%20hypothyroidism
So, reintroducing insulin in the context of low-carb i.e. low-insulin environment, the number of receptors in the liver increases. Look analoguous to glut4 reseptors being invited to cell surface by insulin.
This should go both ways, explaining the high-responders rise of ldl when going to keto.
JR
I need to study up on this a bit. I guess. Sigh. Long ago I determined (to my own satisfaction, at least) that lipids don't play much, if any, role in heart disease and that the lipid hypothesis was incorrect. Since then, I have avoided spending much time reading about lipids, especially since there is so much other really interesting and important stuff to read about.