00:01
One different mutations and two different treatments.
00:04
You have su treatment, you have dg mutation.
00:07
So from a graph, you can see that.
00:10
Su treatment is going to induce increase insulin secretion.
00:20
Because as you can see from the figure, even when the blood sugar level is low at fasting, the insulin secretion of beta cell treated with su increases.
00:37
So even in fasting condition, it increased.
00:42
Let's look at djg.
00:45
Djg mutant has the opposite effect.
00:49
It inhibits insulin secretion even at maximum blood sugar level.
01:06
Usually in wild type, you can see the incidence of frequency increases.
01:10
So these two are the data that we get from our graph.
01:13
So let's fill in a blank.
01:14
So first of all, let's talk about this su.
01:19
The first blank is regarding the su treatment.
01:25
So since it increased the secretion of insulin, it must be an activator.
01:40
So the activator activate the channel.
01:44
So what kind of channel? so according to our knowledge, the insulin secretion is caused or is activated by the by the potassium controlled depolarization gated.
01:57
So the depolarization gated channel actually opened and caused depolarization, which triggered insulin secretion.
02:05
So the second blink is a depolarization gated.
02:31
And when we talk about depolarization, this means the increase of memory potential.
02:36
And this depolarization is actually triggered by the potassium ion.
02:41
So the third link is so when the potassium, the extracellular, potassium ion moved in, it caused membrane potential to increase...