Blood Glucose and Glycolysis

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Myster Ycongo

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It might be because I'm delirious, but I just needed a quick clarification regarding blood sugar levels and glycolysis.

If blood sugar is high, because insulin is no longer being made, we would have decreased glycolysis, correct? Glycolysis is limited because glucose cannot get to the cells, right?

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It might be because I'm delirious, but I just needed a quick clarification regarding blood sugar levels and glycolysis.

If blood sugar is high, because insulin is no longer being made, we would have decreased glycolysis, correct? Glycolysis is limited because glucose cannot get to the cells, right?

Glycolysis isn't limited. There's way too much glucose in the body. Glucose transporters become saturated and most of the glucose remains in the blood stream.
 
It might be because I'm delirious, but I just needed a quick clarification regarding blood sugar levels and glycolysis.

If blood sugar is high, because insulin is no longer being made, we would have decreased glycolysis, correct? Glycolysis is limited because glucose cannot get to the cells, right?

In diabetics, you see less glucose utilization. Rather fats are broken down in the liver via beta oxidation and converted from two carbon units (acetate) to ketone bodies. Ketone bodies exit the liver and enter tissues in need and are converted back to acetyl coa which is a citric acid intermediate to be used for energy.
 
Thank you for both your explanations. I guess I was trying to understand why glycolysis would be reduced in this particular case. Let's say we have high blood sugar because insulin is no longer functioning. That means we need to have a way to reduce sugar levels in our blood. What exactly is glycolysis' role in reducing this sugar? Does it have any type of role in blood sugar glucose reduction?
 
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Thank you for both your explanations. I guess I was trying to understand why glycolysis would be reduced in this particular case. Let's say we have high blood sugar because insulin is no longer functioning. That means we need to have a way to reduce sugar levels in our blood. What exactly is glycolysis' role in reducing this sugar? Does it have any type of role in blood sugar glucose reduction?

I believe there is a regulation step during the first or second step or glycolysis which has to do with the enzymes involved in the process. It has something to with feedback inhibition. Too much ATP inhibits the enzyme (phosphofructokinase or hexokinase) and prevents more glucose from being consumed. When ATP levels drop again, there's less inhibition and Glucose gets consumed. I could be wrong so you might want to check up on this.
 
This is from Wikipedia:

Regulation:

The three regulated enzymes are hexokinase, phosphofructokinase, and pyruvate kinase. The flux through the glycolytic pathway is adjusted in response to conditions both inside and outside the cell. The rate in liver is regulated to meet major cellular needs: (1) the production of ATP, (2) the provision of building blocks for biosynthetic reactions, and (3) to lower blood glucose, one of the major functions of the liver. When blood sugar falls, glycolysis is halted in the liver to allow the reverse process, gluconeogenesis. In glycolysis, the reactions catalyzed by hexokinase, phosphofructokinase, and pyruvate kinase are effectively irreversible in most organisms. In metabolic pathways, such enzymes are potential sites of control, and all three enzymes serve this purpose in glycolysis.
 
Thank you for both your explanations. I guess I was trying to understand why glycolysis would be reduced in this particular case. Let's say we have high blood sugar because insulin is no longer functioning. That means we need to have a way to reduce sugar levels in our blood. What exactly is glycolysis' role in reducing this sugar? Does it have any type of role in blood sugar glucose reduction?

Glycolysis is the process by which glucose is broken down into pyruvate in each of our cells. Pyruvate can become acetyl-CoA, which can be used in the Kreb's cycle or fatty acid synthesis. Glycolysis, however, occurs in the cytosol, and insulin deficiency or resistance will prevent much of the glucose from entering cells in the first place. Therefore it's best to say that insulin plays a role in blood sugar reduction, not glycolysis.

That said, only muscle and fat cells require insulin to take in glucose (these cells have insulin-dependent GLUT4 (glucose transporter 4)). Glucose can still be transported by the many other glucose transporters, as well as into the brain (which has no glucose transporters). If glucose levels are very high, it will also be excreted from the body in the urine.

In short: insulin-deficiency reduces the amount of glucose entering cells, thereby reducing the amount of glycolysis.
 
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Thank you for both your explanations. I guess I was trying to understand why glycolysis would be reduced in this particular case. Let's say we have high blood sugar because insulin is no longer functioning. That means we need to have a way to reduce sugar levels in our blood. What exactly is glycolysis' role in reducing this sugar? Does it have any type of role in blood sugar glucose reduction?

While glycolysis is the first step in the production of ATP for the body, it also maintains blood glucose homeostasis. The process differs from tissue to tissue. In muscle and fat tissue, the transporter GLUT4 is insulin-dependent. Cells that use the insulin-dependent transporter GLUT4 store them in vesicles inside the cytoplasm. When insulin binds to receptors on the plasma membrane, the vesicles containing the transporters fuse with the plasma membrane and the transporters are made available to shuttle the glucose across the plasma membrane into the cytosol, where it can be used in glycolysis. I would provide you with the links to the documents I used, but since this is my first post, I do not have the privilege to use links.

While the GLUT4 transporter is insulin-dependent, its underexpression or overexpression may be more or just as important as the presence of insulin. Read this quote:

"Conversely, conditional depletion of GLUT4 in either adipose tissue or skeletal muscle causes insulin resistance and a roughly equivalent incidence of a diabetic animal."

The rats also displayed different characteristics depending on which tissue was GLUT4-deficient.
 
Are you talking specifically about in insulin-resistant diabetes? In insulin-resistant diabetes, your blood sugar is high because your cells can't respond to the insulin (which causes, among other things, translocation of GLUT to the membrane to import glucose) and so they're starved for glucose. That's why you get such things as diabetic ketoacidosis.
 
Are you talking specifically about in insulin-resistant diabetes? In insulin-resistant diabetes, your blood sugar is high because your cells can't respond to the insulin (which causes, among other things, translocation of GLUT to the membrane to import glucose) and so they're starved for glucose. That's why you get such things as diabetic ketoacidosis.
No, I was describing the function of glucose transporter-4 (GLUT4) in general, how it is insulin-dependent, and how it is responsible for blood glucose homeostasis, since an underexpression of GLUT4 could conceivably create insulin resistance. In addition, an article on the relationship between liver cirrhosis and diabetes-2, states, "Glucose transporter-4 (GLUT4), one of the most important glucose transporters, plays a key role in the development of type 2 diabetes." One caveat: the article was discussing patients with early and advanced liver cirrhosis and diabetes-2, not just patients who had diabetes-2. (source found at ncbi.nlm.nih.gov/pmc/articles/PMC3150722/)
 
No, I was describing the function of glucose transporter-4 (GLUT4) in general, how it is insulin-dependent, and how it is responsible for blood glucose homeostasis, since an underexpression of GLUT4 could conceivably create insulin resistance. In addition, an article on the relationship between liver cirrhosis and diabetes-2, states, "Glucose transporter-4 (GLUT4), one of the most important glucose transporters, plays a key role in the development of type 2 diabetes." One caveat: the article was discussing patients with early and advanced liver cirrhosis and diabetes-2, not just patients who had diabetes-2. (source found at ncbi.nlm.nih.gov/pmc/articles/PMC3150722/)

I think you have it backwards - insulin dependence causes GLUT4 underexpression since insulin itself is what causes translocation of GLUT4 to plasma membranes.
 
I think you have it backwards - insulin dependence causes GLUT4 underexpression since insulin itself is what causes translocation of GLUT4 to plasma membranes.

Cells that use the insulin-dependent transporter GLUT4 store it in vesicles inside the cytoplasm. When insulin binds to receptors on the plasma membrane, the vesicles containing the transporter fuse with the plasma membrane. The transporter then shuttles the glucose across the plasma membrane into the cytosol of the cell, where it can be used in glycolysis. If GLUT4 is artificially underexpressed, for example, in knock-out mice, the mice experience insulin resistance. On the other hand, if GLUT-4 were purposely overexpressed, the mice's insulin resistance was overcome. Please read at sciencedirect page and use the qualifiers "/science/article/pii/S1550413107000678".
 
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