TBR endocrinology & immunology, question #88; effects of GIP

[tdod]

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Why would insulin lead to glucose catabolism? I know that insulin triggers glucose uptake, but shouldn't we expect the cell's utilization of glucose to depend on the needs of the cell? For example, isn't it entirely possible that the insulin stimulates glycogenesis, rather than glycolysis?

Also, why does insulin "promote utilizing glucose as a fuel source"? Doesn't insulin also promote the uptake of amino acids and free fatty acids?


–Thanks!

 

[orangetea]

So the clue here is in the first sentence "GIP is known to mimic certain Insulin responses"

What I remember is:

1. When glucose is up Insulin is up
2. When glucose is down Glucagon is up

Therefore, since Insulin uses the excess glucose as fuel for the cell it would NOT inhibit the enzymes used in the pathway (cross out A and B). C is wrong because Glucagon is the hormone in charge of glycogen breakdown, which leaves us with D.

Like the answer choice says, Insulin works to use glucose as a source of fuel for the cell. Here's more in depth biological steps that take place (I found it on wiki)

Beta cells in the islets of Langerhans release insulin in two phases. The first phase release is rapidly triggered in response to increased blood glucose levels. The second phase is a sustained, slow release of newly formed vesicles triggered independently of sugar. The description of first phase release is as follows:

• Glucose enters the β-cells through the glucose transporter, GLUT2.
• Glucose goes into glycolysis and the Krebs cycle, where multiple, high-energy ATP molecules are produced by oxidation, leading to a rise in the ATP:ADP ratio within the cell.
• An increased intracellular ATP:ADP ratio closes the ATP-sensitive SUR1/Kir6.2 potassium channel (see sulfonylurea receptor). This prevents potassium ions (K+) from leaving the cell by facilitated diffusion, leading to a buildup of potassium ions. As a result, the inside of the cell becomes more positive with respect to the outside, leading to the depolarisation of the cell surface membrane.
• On depolarisation, voltage-gated calcium ion (Ca2+) channels open which allows calcium ions to move into the cells by facilitated diffusion.
• An increased intracellular calcium ion concentration causes the activation of phospholipase C, which cleaves the membrane phospholipid phosphatidyl inositol 4,5-bisphosphate into inositol 1,4,5-trisphosphate and diacylglycerol.
• Inositol 1,4,5-trisphosphate (IP3) binds to receptor proteins in the plasma membrane of the endoplasmic reticulum (ER). This allows the release of Ca2+ ions from the ER via IP3-gated channels, and further raises the intracellular concentration of calcium ions.
• Significantly increased amounts of calcium ions in the cells causes the release of previously synthesized insulin, which has been stored in secretory vesicles.

 

[funtertaining15]

A and B are part of the same pathway in going from glucose--->pyruvate [ hexokinase adds a phosphate to glucose so cells keep taking it in, thinking they're low on glucose, a little trick; PFK I believe is responsible for converting fructose 6 phos to fructose bisphosphate...both enzymes add phosphates ] (Biochem knowledge), so that leaves you with C and D. Insulin is responsible for decreasing BLOOD GLUCOSE LEVELS, so glucose moves into cells and is converted into glucose storage, like in the form of glycogen. GIP would not stimulate glycogen breakdown since you'd be releasing glucose into the blood, which is the opposite of what insulin does (that's glucagon's job), so you're left with D. Basically, insulin indirectly would convert the glucose in the blood for energy and or storage once glucose enters the cells. 🙂

 

[Shirafune]

I was a little bit confused at first, so I understand what you're suggesting, but I don't think you need to analyze the problem this much. I did not know that insulin increases glucose catabolism, but I did know that beta cells in the pancreas release it in response to high plasma glucose levels. It is also responsible for increasing glycogen storage in the liver and muscles.

You really only needed the "mimic certain insulin responses." Here's what I thought about when eliminating answers:

(A) hexokinase phosphorylates glucose in glycolysis (glucose to G6P). Inhibition of hexokinase would lead to a build up of glucose, since insulin is released in relatively high amounts of during high plasma glucose levels. You would not want to inhibit glycolysis when you have lots of glucose around.

(B) Similar reason for elimination as (A). Phosphofructosekinase phosphorylates F6P to F1,6BP. Inhibition of glycolysis when you have a lot of free glucose is not preferred.

(C) Excess glucose is stored as glycogen in the liver and muscles. Stimulation of glycogen (glucose stores) breakdown does not make sense when you have excess glucose around.

(D) This is the only step that makes sense when you have high levels of glucose: increased metabolism.