DammitLetMeIn said:
docj077 said:
It's not insulin that does the damage. In fact, insulin prevents the damage. Low levels of insulin will cause hyperglycemia. Hyperglycemia causes cells and tissues that don't have insulin receptors to take up the excess sugar. Increased glucose within the cell results in the glucose being converted to sorbitol. Sorbitol is the molecule responsible for glycosylation of proteins including cellular enzymes. Not only that, but these sugars can form reducing sugars and damage other cellular structures.
When insulin is around this whole process is avoided unless there is insensitivity at the level of the insulin receptor which happens to be a tyrosine kinase. The predisposition to towards developing this insensitivity is largely genetic in origin.
So this Doctor's (and many many others) are wrong and you (a mere medical student) is right?
Why is your screen name Doctor when your not a doctor. Thats misleading.
No, the doctor is correct if you simply read another paragraph down. Your interpretation is once again incorrect.
You want the mechanism, here is the mechanism.
"Intracellular Hyperglycemia with Disturbances in Polyol Pathways. In some tissues that do not require insulin for glucose transport (e.g. nerves, lenses, kidneys, blood vessels), hyperglycemia leads to an increase in intracellular glucose that is then metabolized by the enzyme aldose reductase to sorbitol, a polyol, and eventually to fructose. In this process, intracellular NADPH is used as a cofactor. NADPH is also required as a cofactor by the enzyme glutathione reductase for regenerating reduced glutathione (GSH). You will recall that GSH is one of the important antioxidant mechanisms in the cell, and a reduction in GSH levels increases cellular susceptibility to oxidative stress. In the face of sustained hyperglycemia, progressive depletion of intracellular NADPH by aldol reductase leads to a compromise of GSH regeneration. Thus, the deleterious consequences of the aldose reductase pathway arise primarily by increasing cellular susceptibility to oxidative stress(1)."
1.Kumar, Abbas, and Fausto. Robbins and Cotran Pathologic Basis of Disease. 7th Edition. Copyright 2005. PG. 1198-1199.
If you have questions regarding the validity of the material presented here, check the comments and rating regarding this book. There is only one book required for medical school pathology. This is the book. Not only that, but this entire book controls the future of any aspiring M.D. as it's the only book that will allow you to pass pathology. Pathology makes the doctor.
Since you seem to inclined to study science and utter your simplistic interpretations of scientific theory, perhaps you should read this book. It's only 1446 pages long and if you're a brave person, you'll realize that a medical student is tested over every single word.
http://www.amazon.com/Robbins-Cotran-Pa ... 460&sr=8-1
So, like I said, the majority of the damage takes place in tissues that do not require insulin for the uptake of glucose. Not only is this true, but the correlation between obesity and insulin resistance is very high, as well as, the correlation between insulin resistance and genetic inheritance.
Unfortunately, not everyone on these forums has insulin resistance. The physical signs and symptoms are quite easy to diagnose if you know what your body feels like when it goes hyper- or hypoglycemic in different situations.
And my screen name is "Doctor", because that's the nickname my grandfather gave me before he passed away from complications due to Glioblastoma multiforme you inconsiderate dick. Two months from diagnoses to death. You really are an a**h**. Congrats on that accomplishment.
