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| Home | Polyol pathway, neuropathy, myo-inositol, t2d, etc | Decreased collagen production with t2d, bone fragility, etc. | Low ascorbate is more significant than glycation in t2d | abnormalities of ascorbic acid metabolism and t2d | Ascorbate supplement recommended for t2d--2 grams | ascorbate polyol pathway abnormal metabolism et. | ascorbate deficiency reduced collagen polyol pathway | Insulin Resistance and Atherogenesis |
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recommended COLLAGEN, ASCORBATE (vitamin C) |
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Polyol pathway, neuropathy, myo-inositol, t2d, etc
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“Also called the sorbitol-aldose reductase pathway, the polyol pathway appears to be implicated in diabetic complications, especially in
microvascular damage to the retina,[1] kidney,[2] and nerves.[3] Sorbitol cannot
cross cell membranes, and, when it accumulates, it produces osmotic stresses on cells by drawing water into the insulin-independent tissues.[4] Cells use glucose for energy. This normally occurs by phosphorylation
via the enzyme hexokinase. However, if large amounts of
glucose are present (as in diabetes mellitus), hexokinase becomes
saturated and the excess glucose enters the polyol pathway when aldose
reductase reduces it to sorbitol. Sorbitol dehydrogenase can then oxidize sorbitol to fructose, which produces NADH from NAD+. Hexokinase can return the molecule to the glycolysispathway by phosphorylating fructose to form fructose-6-phosphate….
While most cells require the action of insulin for glucose to gain entry into
the cell, the cells of the retina, kidney, and nervous tissues are insulin-independent, so glucose
moves freely across the cell membrane, regardless of the action of insulin. [This is not pathological as proven by the very high
carbohydrate diets of the Highland New Guinea peoples, the Japanese and Katovans.]
The cells will use glucose for energy as normal, and any glucose not used for
energy will enter the polyol pathway. When blood glucose is normal (about 100 mg/dl or 5.5 mmol/l), this interchange
causes no problems, as aldose reductase has a low affinity for glucose at normal concentrations” Wiki. ANOTHER PHARMA SUPPORTIVE
ARTICLE STRESSING HIGH GLUCOSE, GLYCATION,
OXIDATIVE DAMAGE, WHILE NOT MENTIONING COLLAGEN, LET ALONE DEFECTIVE COLLAGEN. And
it gets worse in that in the article on collagen there is no mention of
diabetes. Synthesis
“First, a
three-dimensional stranded structure is assembled, with the amino acids glycine
and proline as its principal components. This is not yet collagen but its
precursor, procollagen. Procollagen is then modified by the addition of hydroxylgroups to the amino acids proline and lysine. This step is important for later glycosylation and the formation of the triple helix structure of
collagen. Because the hydroxylase enzymes that perform these reactions require vitamin C as a cofactor, a long-term deficiency
in this vitamin results in impaired collagen synthesis and scurvy.[20] These hydroxylation
reactions are catalyzed by two different
enzymes: prolyl-4-hydroxylase[21] and lysyl-hydroxylase.
Vitamin C also serves with them in
inducing these reactions. In this service, one molecule of vitamin C is destroyed
for each H replaced by OH. [22] The synthesis
of collagen occurs inside and outside of
the cell. The formation of collagen which results in fibrillary collagen (most
common form) is discussed here. Meshwork collagen, which is often involved in
the formation of filtration systems, is the other form of collagen. All types
of collagens are triple helices, and the differences lie in the make-up of the
alpha peptides created in step” https://en.wikipedia.org/wiki/Collagen.
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