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Polyol (sorbitol) pathway and consequences
The sorbitol or polyol pathway is a two-step metabolic pathway that converts glucose into fructose.
Normally, glucose is processed by the glycolysis pathway and is utilized for ATP production and energy. When glucose levels become exorbitantly elevated, other pathways are upregulated to handle the glucose effectively. These pathways include the glycation pathway, the hexosamine pathway, the protein kinase C pathway, the alpha-ketoaldehyde pathway, and the sorbitol/polyol pathway.

First step
The first step in the sorbitol pathway is the conversion of glucose to sorbitol via the enzyme aldolase reductase. This step utilizes a hydrogen group donated by NADPH. This is also the rate-limiting reaction of this entire pathway.

Oxidative stress: All of these pathways that are upregulated in case of exorbitantly elevated glucose levels result in reactive oxygen species (ROS).
Osmotic stress leading to cataract and kidney issues: A point of concern regarding the sorbitol pathway is that not all tissues have the enzyme sorbitol dehydrogenase, and these include the retina, kidneys, and Schwann cells. As a result, in diabetic patients or those with extremely high glucose levels, sorbitol accumulates to toxic levels. Sorbitol and fructose are both practically membrane impermeable. In these tissues without sorbitol dehydrogenase, accumulation of sorbitol intracellularly draws fluid into the tissues leading to elevated osmotic stress. This hypothesis is the prevailing explanation for why cataract formation occurs in the lens, which has a low level of sorbitol dehydrogenase activity. In mice that overexpress aldolase reductase combined with having a sorbitol dehydrogenase deficiency phenotype, elevated glucose levels resulted in a quicker rate of lens sorbitol accumulation and subsequent cataract formation. Additionally, due to the lack of sorbitol dehydrogenase, sorbitol accumulation can impair kidney function. Studies have shown that sorbitol accumulation intracellularly leads to enzymuria and proximal tubular cell dysfunction.
Demyelination of perpheral nerves: Sorbitol accumulation also impairs Schwann cell function. Schwann cells are responsible for the myelination of peripheral nerves. Sorbitol accumulation results in Schwann cell de-differentiation to immature cells and a decreased expression of IGF-1 in the cells.
Glutathione: There is competition for NADPH between glutathione reductase and aldolase reductase. As such, high glucose impairs glutathione recyling. As a result, we can expect detoxification issues and increased oxidative stress.

Second step
The second step in this pathway is the conversion of sorbitol into fructose via the enzyme sorbitol dehydrogenase.  This step donates a hydrogen group to NAD+, creating a byproduct of NADH. This step is reversible.

High fructose leads to ATP depletion: As the polyol pathway continues to metabolize glucose, an overproduction of fructose in the body occurs. This has several metabolic consequences. The surplus of fructose is metabolized by fructokinase, which requires ATP. This results in acetyl-CoA overproduction and depletion of ATP.
Impairing protein function: Overproduction of acetyl-CoA can impair protein function by causing protein acetylation. Fructose also can chemically glycate proteins via fructose metabolism byproducts fructose-3-phosphate and 3-deoxyglucose, impairing protein function.
NAFLD: The surplus in acetyl-CoA has the potential to cause non-alcoholic fatty liver disease since acetyl-CoA is a precursor molecule to fatty acids.
Damage to sperm, small intestine and kidneys: The glucose transporter, GLUT5, is responsible for the transport of free fructose and is found on spermatocytes, small intestinal enterocytes, and kidneys for further metabolism. Overproduction of fructose and subsequent transport through the GLUT5 into these organs can cause further damage.
Triglyceride increase: Fructose is metabolized by the liver, where it stimulates de novo lipogenesis. The triglycerides synthesized lead to hepatic insulin resistance and dyslipidemia.

Glucose, sorbitol and fructose are also related to Alzheimer's, as all three are markedly elevated in all Alzheimer brain regions.