Diabetes mellitus oxidation state

The effect of PJ consumption by patients with CAS on their serum oxidative state was measured also as serum concentration of antibodies against Ox-LDL.31 A significant (p < 0.01) reduction in the concentration of antibodies against Ox-LDL by 24 and 19% was observed after 1 and 3 months of PJ consumption, respectively (from 2070 61 EU/mL before treatment to 1563 69 and 1670 52 F.lI/mL after 1 and 3 months of PJ consumption, respectively). Total antioxidant status (TAS) in serum from these patients was substantially increased by 2.3-fold (from 0.95 0.12 nmol/L at baseline up to 2.20 0.25 nmol/L after 12 months of PJ consumption). These results indicate that PJ administration to patients with CAS substantially reduced their serum oxidative status and could thus inhibit plasma lipid peroxidation. The susceptibility of the patient s plasma to free radical-induced oxidation decreased after 12 months of PJ consumption by 62% (from 209 18 at baseline to 79 6 nmol of peroxides/milliliter). The effect of PJ consumption on serum oxidative state was recently measured also in patients with non-insulin-dependent diabetes mellitus (NIDDM). Consumption of 50 mL of PJ per day for a period of 3 months resulted in a significant reduction in serum lipid peroxides and thiobarbituric acid reactive substance (TBAR) levels by 56 and 28%, respectively.32... 

Chromium in the +3 oxidation state is an essential trace element (see Section 10.3) required for glucose and lipid metabolism in mammals, and a deficiency of it gives symptoms of diabetes mellitus. However, chromium must also be discussed as a toxicant because of its toxicity in the +6 oxidation state, commonly called chromate. Exposure to chromium(VI) usually involves chromate salts, such as Na2Cr04. These salts tend to be water soluble and readily absorbed into the bloodstream through the lungs. The carcinogenicity of chromate has been demonstrated by studies of exposed workers. Exposure to atmospheric chromate may cause bronchogenic carcinoma with a latent period of 10 to 15 years. In the body, chromium(VI) is readily reduced to chromium(III), as shown in Reaction 10.4.3 however, the reverse reaction does not occur in the body. 

Because insulin normally inhibits lipolysis, a diabetic has an extensive lipolytic activity in the adipose tissue. As is seen in Table 21.4, plasma fatty acid concentrations become remarkably high. /3-Oxidation activity in the liver increases because of a low insulin/glucagon ratio, acetyl-CoA carboxylase is relatively inactive and acyl-CoA-camitine acyltransferase is derepressed. /3-Oxidation produces acetyl-CoA which in turn generates ketone bodies. Ketosis is perhaps the most prominent feature of diabetes mellitus. Table 21.5 compares ketone body production and utilization in fasting and in diabetic individuals. It may be seen that, whereas in the fasting state ketone body production is roughly equal to excretion plus utilization, in diabetes this is not so. Ketone bodies therefore accumulate in diabetic blood. 

In diabetes mellitus, blood glucose homoeostasis and rate of lipolysis in adipose tissue appear to be associated. This relationship is most apparent in an insulin-deficient state, where glucose homoeostasis is maintained at the expense of other fuel sources, mainly FFA. Insulin deficiency initiates lipolysis. The increase in fatty acid oxidation further favours hepatic gluconeogenesis. 

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