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And you can also change the quality settings to the highest one for better graphics. Let's talk about insulin. Insulin is a polypeptide hormone.
And as I mentioned, it has a major role in the regulation. of macromolecules within our body and has a major role in the homeostatic condition of metabolism. But the main role insulin has is in storing excess energy, as in storing fats, lipids, carbohydrates, and proteins, such as during a fed state. So now I would like to show you the associated organs insulin has an effect on. So for example here we have the intestines, here we have the blood, here we have the liver, Skeletal muscle, lymphatic circulation, adipose tissue, and finally the last organ, the pancreas.
Now insulin has a major effect during the fed state, so basically just after we eat. Because after we eat, we would have many macromolecules running through our intestines, such as glucose here, amino acids, and then we also have fats. Now let's concentrate on glucose first. What happens here? Well, glucose will be absorbed by the blood.
and the pancreas will then secrete insulin. And insulin will promote the uptake of glucose from the blood into the liver. Insulin will also promote the conversion of glucose to glycogen, the storage unit of glucose.
Insulin will promote the conversion of glucose to pyruvate and then to acetyl-CoA by glycolysis. Insulin will promote acetyl-CoA to triacylglycerols. And then, trisoglycerols can then be packaged up into very low density lipoproteins, which can then be stored as trisoglycerol in adipose tissue.
So insulin does all these things. Insulin also has effect on amino acids. Amino acids will be absorbed by the blood. Insulin will promote the uptake of amino acids from the bloodstream to the liver. And then insulin will promote protein protein proteogenesis so therefore promoting protein synthesis insulin also has effects on fats but fats are absorbed through the lymphatic circulation not through the blood and insulin will promote uh the storage of fats within skeletal muscle as fatty acids insulin also promote the synthesis of triacylglycerol from fat in the liver so that was a brief overview of the effects insulin has on the different types of organs in our body and as you can see insulin has the major role of storing excess energy, such as during the fed state, when we have a lot of macromolecules running through our intestines that need storing.
So now let's look at insulin synthesis. And insulin synthesis occurs in the pancreas, but particularly in the beta cells of the pancreas, because it is within these beta cells that insulin is secreted from. So let's begin with the ribosome, which translates mRNA into a particular protein.
And this protein is actually for insulin. So this protein will form what's called a pre-proinsulin, which is a long polypeptide. And then this pre-proinsulin will get transported into the endoplasmic reticulum, where it will get sorted out and cleaved up a bit to form proinsulin.
And the proinsulin consists of three segments, A, C in the middle, and B. Now, this proinsulin will then travel to the Golgi apparatus, where it will get cleaved up into the associated segments. The C-peptide, which is in the middle, and also the A and B-peptide, which will form insulin.
The A and B-peptide will be bounded together by disulfide bonds, and this is what insulin is. So insulin is connected by disulfide bonds from the A and B-peptides from pro-insulin. And the C-peptide will then travel to... C-peptide has a role in the cell membrane for G-protein signaling in some way. So this insulin can then be secreted into the bloodstream, where it will travel to its target tissue or associated organs.
Now, for example, it will travel to the liver, let's just say. Or it can travel to the skeletal muscle. So now let's zoom into the membranes of the skeletal muscle and liver. So the membranes are obviously different, but the insulin receptor is the same. Because insulin receptor is a tyrosine.
kinase receptor. and it consists of two alpha subunits, two beta subunits, and tyrosine kinase in the intracellular fluid, in the inside. Tyrosine kinase is an enzyme, and it's inactive when it's not phosphorylated, when it doesn't have a phosphate group. But usually, tyrosine kinase has autophosphorylation, which means that it always has a phosphate group. So tyrosine kinase, when it has a phosphate group coming off it, it is active.
Okay, now within the... with inside the cell in the cytosol in the intracellular fluid there's a target protein with with a tyrosine amino acid for example and this target protein is inactive when it's not phosphorylated so how does it become active and how does the tyrosine kinase receptor the insulin receptor become stimulated well when insulin travels to the target organ for example the liver the two insulins will have to bind to the two alpha subunits, which will then cause tyrosine kinase to phosphorylate the target protein in the inside of the cell. So this target protein will become phosphorylated. It will have the phosphate group attached to the tyrosine amino acid. And now, because this target protein is phosphorylated, it is active.
And so because it is active, it can then cause the intracellular effects of insulin. I hope you understood that. That was a...
brief overview, but now let's look at this tyrosine kinase receptor in a bit more detail. So let's look at it again in a more bigger picture. So here we have the liver.
We'll cut a cross section here and look at one of the cell of the hepatocytes, the cell membrane of the hepatocytes. So the tyrosine kinase receptor, which is for insulin, the insulin receptor, consists of four subunits. and two inner enzymes.
So it consists of two alpha subunits, two beta subunits, and two intracellular tyrosine kinase, bound to the beta subunits on the inner membrane. And the tyrosine kinase is autophosphorylated, so it contains many phosphate groups. The alpha and beta subunits, as well as the alpha and alpha subunits, are connected by disulfide bonds.
Once insulin binds to the alpha subunits, there needs to be two insulin binding to the alpha subunits, it will cause an... an inner membrane protein known as IRS1 to be phosphorylated. And this will activate IRS1, which is the target protein. IRS1, once phosphorylated, has many effects on that particular cell.
Such as, it will promote growth for gene expression. IRS also promotes glycogen synthesis. for storage of glucose. IRS-1, once phospholipid, will also promote fat synthesis, so the synthesis of triglycerols. IRS-1 will also stimulate protein synthesis.
Once it absorbs amino acids, it will make proteins. And also importantly, IRS-1 will increase the expression of glucose transporters. What this means is that glucose transporters in the inner membrane will travel out to the plasma membrane, to the outer membrane.
And And in this case, the liver has a special glucose transporter called GLUT2. Now it should be noted here that diabetes or, mainly, insulin resistance is a condition when insulin itself cannot bind to the tyrosine kinase receptor and therefore IRS cannot increase the expression of glucose transporters and therefore glucose just accumulates in the bloodstream, increasing blood glucose levels. And so liver, as I mentioned, expresses specifically type 2 glute transporters.
Other organs has different glute transporters, like the muscle has glute 4. Anyway, the increased expression of glute 2 transporters will increase the absorption of glucose from the bloodstream into the liver. So glucose is inside the liver now. And glucose can then have a number of fates.
It can be stored as a glycogen, as in glycogen synthesis, or it can be converted to fats, which will then be packaged up as VLDLs, very low density lipoproteins, or lipoproteins in general, and to be exported into the adipose tissue to be as well stored. So insulin, now let's look at the broad picture here. So insulin essentially lowers blood glucose levels as well as as well as it stimulates the absorption and storage of excess energy.
So let's go over the major effects insulin has in the body. So insulin inhibits the degradation of glycogen to glucose. So it inhibits glycogen phosphorylase, the enzyme responsible for this. Insulin promotes glucose, glucose conversion to glucose 6-phosphate, so it stimulates the enzyme hexokinase.
Insulin also stimulates the conversion of glucose 6-phosphate through a series of enzymes to glycogen and so essentially it stimulates glycogen synthase, the enzyme for glycogen synthesis. Insulin also increases the expression of glucose transporters in the liver, so increases glucose transport to the liver, so increases GLUT2 transporters. Also insulin increases the expression of GLUT2 transporters. for transporters in the muscle and adipose tissue. Insulin also stimulates ribosome activity to synthesize proteins, so protein synthesis.
Insulin also inhibits, particularly, protein degradation because it wants to store excess energy. It wants to store amino acids. Insulin also promotes the conversion from glucose to acyl-CoA, so. It promotes glycolysis, as well as insulin promotes fatty acid synthesis from acetyl-CoA to triacylglycerols.
And finally, insulin also inhibits hormone-sensitive lipase, which is responsible for the degradation of triacylglycerols to fatty acids. Of course, insulin also prevents beta-oxidation, the conversion of fatty acids into acetyl-CoA. In summary, insulin is important in storing excess energy. in the forms of glycogen, triglycerols, and proteins in different organs. And that concludes basically this video on insulin.
Please watch the video on glucagon if you haven't watched it yet. Please comment, like, and subscribe. Thank you very much.