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Home | Fructose the starting point | Low Carb diet to treat type-2 diabetes | Bad Medicine Diabetes--Des Spence | Bad Medicine Diabetes--Des Spence | THE CAUSES: Fructose, insulin resistance, ascorbate, and collagen | More Jounral articles on COLLAGEN and its role in diabetic pathologies | Ascorbic acid diabetes studies | Journal articles on polyol pathway and ascorbate | Ascorbate role and not hyperglycemia is pathogenic | Explanatory letter recommending ascorbate supplement
Fructose the starting point

Exposes standards method for measuring glycation of fructose underestimates it rate. Compared two methods of measuring glucose fructose glycation products; it occurred for fructose at a 3 fold great rate for formation of carbonyl, and a 15 fold when using fluorescence intensity.
Journal of Diabetes and its Complications Volume 9, Issue 2, April–June 1995, Pages 87-91
Significance of fructose-induced protein oxidation and formation of advanced glycation end product
To investigate the significance of fructose-induced protein modification, we examined both fructose-and glucose-induced protein oxidation and the formation of advanced glycation end products (AGE) in vitro. Albumin incubated in the presence of 100 mM fructose at 37 C for 1 week showed 5.1-fold and 3.1-fold increases in the content of carbonyl, which is a marker for oxidized protein, when compared with either control incubated without sugar or with 100 mM glucose. Similarly, the same incubation with fructose increased the fluorescence intensity over 100-fold and 15-fold formation compared with that of no sugar and glucose controls, respectively. Both fructose-induced fluorescence and protein oxidation were almost completely suppressed in the presence of the iron chelator; deferoxamine (100 μM), the hydroxyl radical scavenger; MK-447 (1 mM), or aminoguanidine (200 mM), which is an inhibitor of AGE formation. In contrast, the fructose-induced formation of fluorescent albumin was potentiated in the presence of 100 μM FeCl2. This was completely inhibited in the presence of 60 μM or more deferoxamine. These results suggest that fructose promotes both AGE formation and protein oxidation possibly through the formation of hydroxyl radicals.

Kobe J. Med Sci, Vol 48 no 5 pp 125-136, 2002
Experimental Studies on the Role of Fructose in the Development of Diabetic Complications
Supports the finding of Lustig below. This PDF form wont copy. Of interest was a comparison of the extent of glycation of collagen after incubation; for glucose it was 86.9% of the collagen was in tack while with fructose it was 15.9%

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