AKT Signaling Pathway: Regulation by the Insulin Signaling Cascade
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- Опубликовано: 20 окт 2024
- Lesson on the Insulin Signaling Pathway and its Regulation of the AKT Pathway. The insulin signaling cascade is activated upon binding of insulin to the insulin receptor. Afterwards, downstream targets, including IRS1/2, become activated, eventually leading to activation of AKT via two distinct mechanisms and two important phosphorylation sites on AKT. These AKT phosphorylation are important for AKT activation. These two sites also are regulated by two phosphatase enzymes as well. Eventually, activation of AKT will lead to particular effects within the insulin-stimulated cell, which we also discuss in this lesson.
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PDK is not pyruvate dehydrogenase kinase ....it's phosphoinositide dependent protein kinase
Actually 3-phosphoinositide-dependent protein kinase 1
Thsnks, I waited this video for a long time.
Thank you sir
it was really confusing before
Thank you! So, P70S6K inhibiting IRS1/2 phosphorylation would have any relation to insulin resistance?
A bit late to reply, but my 2 cents is that is possibly could be the case.
We know that obesity often happens in concert with insulin resistance. Theoretically, when one is in a chronic calorie surplus (gains weight), that would happen in concert with a lot of insulin secretion (either one is on a high-carbohydrate diet, or their high fat/protein diet would spare carbohydrates from oxidation, allowing for them to induce insulin secretion in the pancreas). A lot of insulin secretion would, in theory, lead to more of the insulin signaling cascade, would could theoretically lead to a lot of p70s6 kinase inhibiting IRS 1/2, serving as the "feedback mechanism" of the insulin signaling cascade, decreasing the "potency" of insulin's metabolic effects (such as clearing glucose from the bloodstream).
I think the "potency" of insulin may possibly be inversely proportional to the activity of p70s6 kinase (which would make theoretical sense, since p70s6 kinase inhibits IRS 1/2), and I think it makes practical sense since weight loss (which would, in theory, lead to less insulin secretion) is generally prescribed to help with insulin resistance.
Just my 2 cents, but hope this helps.
Saw an interesting video from Robert Lustig... is it possible that the liver's insulin receptors can be knocked out / resistant (and disrupt the FOXO pathway), yet *NOT* affect the SREBP-1c pathway?
Hello sir . I need your help sir from where I can get the theory of these pathways
Yeah these things are really complicated 😅😅
thank you so much