Glucose structure and insulin resistance

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mktsgm
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Is there a link between the structure of the glucose and the uptake of glucose into cells
I have a doubt about the process of type-2 diabetes.

It is said that insulin resistance leads to type-2 diabetes. That would mean, even in the presence of insulin, the glucose uptake into the cells does not take place, leading to hyperglycemia.

My doubt is, how could this happen in spite of the presence of insulin?

Could it be something that is structurally wrong with the circulating glucose itself? For example, what happens, if the structure of glucose is changed somehow?

I gather that glucose can exist in different forms such as straight-chain and cyclic ring forms. In cyclic forms also it can be in different isomers such as α-D-glucopyranose, β-D-glucopyranose, α-D-glucofuranose, and β-D-glucofuranose. Also, glucose can convert to mannose also.

I want to know if these structural changes, have anything to do with glucose refusing to enter the cells. Is there any way to detect the changes in the circulating glucose whose uptake is in question?

I would be grateful if any published scientific papers in this regard are shared here.

Thanks
 
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mktsgm said:
TL;DR Summary: Is there a link between the structure of the glucose and the uptake of glucose into cells

I have a doubt about the process of type-2 diabetes.

It is said that insulin resistance leads to type-2 diabetes. That would mean, even in the presence of insulin, the glucose uptake into the cells does not take place, leading to hyperglycemia.

My doubt is, how could this happen in spite of the presence of insulin?

Could it be something that is structurally wrong with the circulating glucose itself? For example, what happens, if the structure of glucose is changed somehow?

I gather that glucose can exist in different forms such as straight-chain and cyclic ring forms. In cyclic forms also it can be in different isomers such as α-D-glucopyranose, β-D-glucopyranose, α-D-glucofuranose, and β-D-glucofuranose. Also, glucose can convert to mannose also.

I want to know if these structural changes, have anything to do with glucose refusing to enter the cells. Is there any way to detect the changes in the circulating glucose whose uptake is in question?

I would be grateful if any published scientific papers in this regard are shared here.

Thanks
I would review what is known about pancreas function first. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5867580/
 
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pinball1970 said:
I would review what is known about pancreas function first. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5867580/
Thanks for the referral. I am quite familiar with the pancreas function.

And just now, while searching for answers to my question, I came across this link.

Anomeric Nature of Glucose and Its Implications

Perhaps this paper is nearly discussing something similar to my doubt "Anomeric Nature of Glucose and Its Implications..."

It discusses the anomers' ratio (between alpha and beta D glucose) with regard to the measurement of glucose.

My doubt lingers if it can somehow relate to the glucose uptake. Just a thought...
 
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It has nothing to do with the structure of glucose, as the two anomers of glucopyranose interconvert rapidly under physiological conditions. Instead, it has to do with the disruption of the pathway that's activated when insulin binds to cellular insulin receptors.

In simple terms: glucose can't cross the cell membrane passively, so in order to get glucose into cells, insulin has to bind to receptors on the outside of those cells. When insulin binds these receptors, it activates a biochemical chain of events which causes the cell to produce proteins that transport glucose across the membrane and into the cell. Insulin resistance occurs when this chain of events gets disrupted. The exact nature of this disruption--which link in the chain gets broken--is still unclear, but there are a number of theories. See also:
https://en.wikipedia.org/wiki/Insulin_resistance#Molecular_mechanism
 
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Related to Glucose structure and insulin resistance

What is the structure of glucose?

Glucose is a simple sugar with the molecular formula C6H12O6. It exists in two primary forms: a linear chain and a ring structure. The ring form is more common in biological systems and can be either alpha (α) or beta (β) depending on the orientation of the hydroxyl group attached to the first carbon atom. In its ring form, glucose is a hexose, meaning it has six carbon atoms, and it typically forms a six-membered ring called a pyranose.

How does glucose enter the cells of the body?

Glucose enters the cells of the body primarily through glucose transporters, which are specialized proteins located in the cell membrane. The most well-known glucose transporter is GLUT4, which is regulated by insulin. When insulin binds to its receptor on the cell surface, it triggers a series of events that cause GLUT4 to move to the cell membrane, allowing glucose to enter the cell from the bloodstream.

What is insulin resistance?

Insulin resistance is a condition in which the body's cells become less responsive to the hormone insulin. As a result, higher levels of insulin are required to achieve the same effect on glucose uptake and metabolism. This can lead to elevated blood glucose levels and is often associated with conditions such as type 2 diabetes, obesity, and metabolic syndrome.

How does insulin resistance affect glucose metabolism?

Insulin resistance affects glucose metabolism by impairing the ability of cells to take up glucose from the bloodstream efficiently. This leads to higher blood glucose levels, which can cause the pancreas to produce more insulin in an attempt to compensate. Over time, the pancreas may become unable to produce enough insulin to maintain normal blood glucose levels, leading to hyperglycemia and the development of type 2 diabetes.

What are the potential causes of insulin resistance?

Insulin resistance can be caused by a variety of factors, including genetic predisposition, obesity, physical inactivity, poor diet, and certain medical conditions. Excessive fat, particularly visceral fat around the abdominal area, is strongly associated with insulin resistance. Inflammation and the release of free fatty acids from adipose tissue can also interfere with insulin signaling pathways, contributing to the development of insulin resistance.

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