Glucose structure and insulin resistance

mktsgm · Aug 24, 2023

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

pinball1970 · Aug 24, 2023

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/

mktsgm · Aug 24, 2023

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...

TeethWhitener · Aug 24, 2023

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

Glucose structure and insulin resistance

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