Relationship Between Rooh And Glycemic Control

Two independent studies from this laboratory have shown no correlation between plasma ROOHs and HbAlc (17,18). On the other hand, there was a scatter association between ROOH and fasting blood glucose (/- = 0.2, p < 0.05) in the diabetic subjects but not in the control group (17,18). ROOH/ cholesterol-standardized a-tocopherol ratio also showed a weak association with fasting blood glucose in the diabetic subjects but not in the control group (r = 0.23, p < 0.05) (18).


Little information is available on the effect of glycemic control on plasma markers of oxidative stress. Berg et al. (26) compared the effect of continuous intensified insulin treatment (CUT) and conventional insulin treatment (CIT) on plasma lipid peroxides as measured by the FOX assay. Plasma ROOHs in patients receiving CIIT fell by 31% as compared with baseline over a period of 24 months. HbAlc fell by 15% during the same period (Fig. 4). By contrast, no difference was seen in patients receiving CIT over the same period. Faure et al. (27) also examined the effect of CIIT on plasma lipid peroxides using the TBA assay. They too reported a marked reduction in TBARs after CIIT as compared with the baseline level (2.42 ± 0.25 vs. 3.03 ± 0.27 (imol/L; n = 16) over a period of 7 years (27). These observations provide further support for the hypothesis of a beneficial effect of insulin therapy on lipid peroxidation brought about by decreasing circulating HbAlc levels


To the best of our knowledge, there is one study addressing the effect of antioxidant therapy on plasma markers of oxidative stress in diabetic patients.

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Figure 4 Change in plasma ROOHs and HbAlc during continuous intensified insulin therapy (CUT) and conventional insulin therapy (CIT).

Borcea et al. (22) studied the effect of the antioxidant a-lipoic acid on plasma ROOHs in diabetic patients (n = 33) receiving a-lipoic acid for 12 weeks (600 mg/day). Diabetics treated with a-lipoic acid had markedly lower levels of plasma ROOHs than the control group. A trend toward higher a-tocopherol concentration was seen in the a-lipoic acid-treated subjects as compared with control subjects. a-Lipoic acid exists naturally in physiological systems as a cofactor for enzymatically catalyzed acyl transfer reactions (28). a-Lipoic acid and its intracellularly reduced form, dehydrolipoate, have been shown to scav enge a variety of reactive species such as HO", ROO", HOC1, and peroxynitrite; to regenerate both a-tocopherol and ascorbate; and to raise intracellular glutathione levels. Thus, these data provide the first direct evidence for the hypothesis that treatment with the antioxidant a-lipoic acid reduces accumulation of ROOHs in the circulation.

Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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