Perfect. Even for a medical student, this was the perfect level of detail for a quick refresh (studying diabetes pharm right now and remembering this pathway is key)
I love the illustration. But what about in the case of an insulinoma? Where the insulin production has nothing to do with how much or how little glucose there is in the blood. Or in the case of a reactive insulinoma or even beta cell hyperplasia where the excessive insulin is provoked by glucose. What starts the process when no sugar is there and what makes the process excessive in its response?
Okay here's my question. Hopefully the body will fill its glycogen stores in the liver and muscles, and then once full deposit excess as fat. Is that how it works? And if so how does that work? There must be some kind of communication level which would allow for the insulin receptors to activate in the fat when the insulin receptors are closed in the liver and muscles.
HI! I'm a little confused about WHY the Ca²+ channels opening leads to Ca²+ influx. The closing of the K+ channels leads to a higher intracellular positive load, so why would positively charged calcium ions go against the load gradiënt?
Hi, thanks for sharing this. My question is, if there is too much insulin production, does this mean that the insulin receptor is malfunctioning and not sending signal back to the pancreas to stop producing insulin? Or something else is responsible for that? Thanks in advance.
@@physiopathopharmaco4190 thanks for answering. If you do the correct diet and stop overloading the receptor, can the receptor recovers over time (maybe with supplements or other way to boost its recovery)and signal the pancreas as it should? So it won’t food the body endlessly with insulin every time someone eats? Or is that regulation has more to do with the Beta cell’s K+&Ca charge regulation? Thanks again.🙏
Actually to me I think increase in insulin secretion leads to low blood glucose levels, hunger,sweating, irritability and double vision yeah that's what my brain and logic Tells me
