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Injury to the pancreas has important metabolic consequences, due to its central role in endocrinological and nutritional homeostasis. Susceptibility of pancreatic tissue to damage by ROS may be due to the relatively low activities of endogenous antioxidant enzymes such as glutathione peroxidase, and comparatively low cellular levels of ATC [93], Certainly, pancreatic islet cells are profoundly sensitive to vitamin E deficiency, as reflected by reduced Mn-superoxide dismutase and increased CuZn-superoxide dismutase activities, coupled with reduced insulin secretory function [94], Pancreatic atrophy due to dietary selenium deficiency can be reversed by high-dose vitamin E supplementation [93],

Experimental pancreatic injury in laboratory animals induced by streptozotocin is a standard model of inducing diabetes. Streptozotocin-induced diabetes alters serum lipidprofiles [95], increases markers oflipid peroxidation such as hepatic thiobarbituric acid reacting substances (TBARS) and conjugated dienes [96-99], and raises serum antibodies against MDA-protein adducts [95], In streptozotocin-induced diabetes, treatment of rats with Vitamin E reduces blood glucose levels and reduces lipid peroxidation [98,99], At the subcellular level, ATC supplementation improves the ability ofhepatic mitochondria to withstand ROS-induced damage in streptozotocin-induced diabetic rats [100].

However, in diabetes, tissue damage is not solely confined to the pancreas, and affected tissues include the eye (both cornea as well as the retina [51]), and kidney [97], Kidney malfunction in diabetes is associated with increased diacylglycerol concentration and protein kinase C activation combined with albuminuria [97], Injection of ATC into streptozotocin-induced diabetic animals impedes these changes, with improved rates of glomerular filtration and urinary albumin excretion rates [97], However, ATC supplementation, whilst increasing hepatic ATC content in mitochondria, does not increase kidney mitochondrial ATC [100], emphasizing the differential uptake of ATC by individual organs.

The therapeutic administration of ATC to diabetic patients has been proposed [101]. Thus, insulin sensitivity of skeletal muscle, a key feature of Type II diabetes, may be improved by ATC supplementation, as a consequence of its ability to increase diacylglycerol kinase, and reduce the phosphatidate phosphohydrolase activity via protein kinase C [97,102], Studies have shown that ATC supplementation for 3 months in diabetic patients reduce plasma TBARS and lipid content [103]: improvements in glucose utilization and liver response to insulin in diabetic patients treated with ATC for 4 months have also been reported [104],

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