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How Does Glucose Get Into A Nerve Cell?
Question: Academic Question.
How does glucose get into a nerve cell?
I know that glucose does not require insulin to open the glucose gate.
I also know that there are proteins on the cell membrane that become glycated and hold the glucose on the surface.
And I have read and seen video on Na/K pumps but I can't find anything on the actual way that the glucose enters the cells.
My question is as a result of discussion on a forum regarding this link http://www.medscape.com/viewarticle/505648_3 but I see that they are picking up the subject without discussing how the "extra" glucose gets in, given that there is extra glucose, which I know is the current thinking.
However nerve cells are very highly active cells all the time, unlike muscle cells. So they would normally have a higher usage of glucose. And they also don't consider that there are many people with long term hyperglycemia who don't develop neuropathy.. I see another important element, which is not considered because it doesn't fit the machine paradigm, and that is belief. Belief of damage can cause damage by an inappropriate immune response. That would explain the higher ROS and damage to the cell.
How does glucose get into a nerve cell?
I know that glucose does not require insulin to open the glucose gate.
I also know that there are proteins on the cell membrane that become glycated and hold the glucose on the surface.
And I have read and seen video on Na/K pumps but I can't find anything on the actual way that the glucose enters the cells.
My question is as a result of discussion on a forum regarding this link http://www.medscape.com/viewarticle/505648_3 but I see that they are picking up the subject without discussing how the "extra" glucose gets in, given that there is extra glucose, which I know is the current thinking.
However nerve cells are very highly active cells all the time, unlike muscle cells. So they would normally have a higher usage of glucose. And they also don't consider that there are many people with long term hyperglycemia who don't develop neuropathy.. I see another important element, which is not considered because it doesn't fit the machine paradigm, and that is belief. Belief of damage can cause damage by an inappropriate immune response. That would explain the higher ROS and damage to the cell.
Brief Answer:
Non insulin depending process
Detailed Answer:
Hi
thank you for trusting HCM
I read you query and I will try to explain something about the process you are interested in
Glucose is a highly reactive compound, and it must be metabolized or it will find tissues in the body with which to react. Increased glucose levels, like those seen in diabetes, activates this alternative biochemical pathway, which in turn causes a decrease in glutathione and an increase in reactive oxygen radicals. The pathway is dependent on the enzyme aldose reductase. Inhibitors of this enzyme have demonstrated efficacy in animal models in preventing the development of neuropathy.
While most body cells require the action of insulin for glucose to gain entry into the cell, the cells of the retina, kidney and nervous tissues are not insulin-dependent. Therefore there is a free interchange of glucose from inside to outside of the cell, regardless of the action of insulin, in the eye, kidney and neurons. The cells will use glucose for energy as normal, and any glucose not used for energy will enter the polyol pathway and be converted into sorbitol. Under normal blood glucose levels, this interchange will cause no problems, as aldose reductase has a low affinity for glucose at normal concentrations.
Hope I have been understandable
Anyway feel free to ask further questions or clarify doubts
Wish you good health
Regards
Dr Eris Ranxha
Neurologist
Non insulin depending process
Detailed Answer:
Hi
thank you for trusting HCM
I read you query and I will try to explain something about the process you are interested in
Glucose is a highly reactive compound, and it must be metabolized or it will find tissues in the body with which to react. Increased glucose levels, like those seen in diabetes, activates this alternative biochemical pathway, which in turn causes a decrease in glutathione and an increase in reactive oxygen radicals. The pathway is dependent on the enzyme aldose reductase. Inhibitors of this enzyme have demonstrated efficacy in animal models in preventing the development of neuropathy.
While most body cells require the action of insulin for glucose to gain entry into the cell, the cells of the retina, kidney and nervous tissues are not insulin-dependent. Therefore there is a free interchange of glucose from inside to outside of the cell, regardless of the action of insulin, in the eye, kidney and neurons. The cells will use glucose for energy as normal, and any glucose not used for energy will enter the polyol pathway and be converted into sorbitol. Under normal blood glucose levels, this interchange will cause no problems, as aldose reductase has a low affinity for glucose at normal concentrations.
Hope I have been understandable
Anyway feel free to ask further questions or clarify doubts
Wish you good health
Regards
Dr Eris Ranxha
Neurologist
Above answer was peer-reviewed by :
Dr. Pradeep Vitta
Thank you for your information. I understand what you are saying but I still have a problem with the level of glucose entering the nerve cells. Because before we can consider oxidative state being excess we need to be convinced that the glucose is not being purposely metabolised at a higher rate owing to inflammatory processes, which I believe are always deliberate, even though misguided at times (eg nocebo simulated events, and what are known as autoimmune).
I have discovered that the glucose enters through GLUT1 or GLUT3 and is aided by the concentration gradient.
I know that if there is extremely low glucose in the external environment the entry of glucose stops but doesn't the cell somehow regulate the excess?
I can see that there are proteins that become glycated, which in a sense are holding the glucose so they must contribute to helping stem the flow into the cells.
I can see that there are plenty of people with diabetes who never get neuropathy or retinopathy or kidney disease. What makes the difference?
There is also my own experience. For instance I have had on a few ocassions inflammatory reactions in association with cancers. The first time I had stage 4 ovarian cancer with extensive metastasis and inflammations AND type 2 diabetes at the same time. It was inoperable and the doctors said 6 months to a year to live. I had a spontaneous remission over a period of 8 months after I left the area I was living in. I found the diabetes, which must have been as a result of the cancer, didn't go away completely until 6 months or so after the cancer was all gone. So I had inflammation that cleared away while I still had high blood sugars. So I am not convinced that the sugar alone is the cause of problems.
How can there be a case to be made that cells do not somehow regulate these transporter and that instead there is a continual flow of glucose into the cell without any address? I found that cells are conscious beings that make decisions eg insulin resistance is a case of deliberately changes, epigenetic changes are deliberate choices.
Thanks Kyrani
I have discovered that the glucose enters through GLUT1 or GLUT3 and is aided by the concentration gradient.
I know that if there is extremely low glucose in the external environment the entry of glucose stops but doesn't the cell somehow regulate the excess?
I can see that there are proteins that become glycated, which in a sense are holding the glucose so they must contribute to helping stem the flow into the cells.
I can see that there are plenty of people with diabetes who never get neuropathy or retinopathy or kidney disease. What makes the difference?
There is also my own experience. For instance I have had on a few ocassions inflammatory reactions in association with cancers. The first time I had stage 4 ovarian cancer with extensive metastasis and inflammations AND type 2 diabetes at the same time. It was inoperable and the doctors said 6 months to a year to live. I had a spontaneous remission over a period of 8 months after I left the area I was living in. I found the diabetes, which must have been as a result of the cancer, didn't go away completely until 6 months or so after the cancer was all gone. So I had inflammation that cleared away while I still had high blood sugars. So I am not convinced that the sugar alone is the cause of problems.
How can there be a case to be made that cells do not somehow regulate these transporter and that instead there is a continual flow of glucose into the cell without any address? I found that cells are conscious beings that make decisions eg insulin resistance is a case of deliberately changes, epigenetic changes are deliberate choices.
Thanks Kyrani
Brief Answer:
Both ok, epigenetic changes
Detailed Answer:
Dear Kyrani
Thank you for coming back again
Unfortunately medicine is just like maths meaning that the result is always the same
In medicine each person is unique, alone in his genetics and type
Anyway in what are you interested most, the first point to be understood, metabolic changes have other mechanism than autoimmune disease
Second, at metabolic changes, damages of nervous system happens after a long time
At your case, examinations need to be controlled, to understand the cause of provoking diabetes
Probably there should be two mechanism, chemotherapy or metastatic changes
In general there are in progress researches to better understand why some people have predisposition to generate symptoms depending on genetic changes of genome
That's the new era of medical sciences
Hope I have clarified some of your doubts
Please feel free to ask for more information or close the query and rate it if you are satisfied
Stay healthy
Regards
Dr Eris
Both ok, epigenetic changes
Detailed Answer:
Dear Kyrani
Thank you for coming back again
Unfortunately medicine is just like maths meaning that the result is always the same
In medicine each person is unique, alone in his genetics and type
Anyway in what are you interested most, the first point to be understood, metabolic changes have other mechanism than autoimmune disease
Second, at metabolic changes, damages of nervous system happens after a long time
At your case, examinations need to be controlled, to understand the cause of provoking diabetes
Probably there should be two mechanism, chemotherapy or metastatic changes
In general there are in progress researches to better understand why some people have predisposition to generate symptoms depending on genetic changes of genome
That's the new era of medical sciences
Hope I have clarified some of your doubts
Please feel free to ask for more information or close the query and rate it if you are satisfied
Stay healthy
Regards
Dr Eris
Above answer was peer-reviewed by :
Dr. Pradeep Vitta
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