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Liver is the primary organ for glucose metabolism. Apart from expressing the enzymes involved in glucose metabolism and regulation, liver possesses numerous enzymes involved in detoxification and toxicity enhancement (Phase I and Phase II). Also, most substances, upon entry into the body are primarily subjected to metabolism in the liver. Several studies have shown that significant oxidative stress and liver damage occurs in diabetes. A study using Non- Obese Diabetic (NOD) mice showed elevated serum enzymes associated with liver damage and apoptosis as indicated by marked DNA fragmentation and all these changes were decreased with selenium treatment. Streptozotocin induced diabetes led to the increased expression of liver and hepatocyte inducible Nitric Oxide Synthase. The activation of Peroxisome Proliferator Activated Receptor alpha (PPAR alpha) was shown to protect STZ treated mice against the toxicity of acetaminophen, a potent hepatotoxicant. Liver mitochondria from STZ-diabetic rats have shown to exhibit less susceptibility to oxidative damage (induced by Fe3+/Adenosine 5’-diphosphate (ADP) xanthine/xanthine oxidase), compared to normal rats. As evidenced through the many studies utilizing in vivo animal models and in vitro models of hepatocytes and HepG2 cells, metabolism of high concentrations of glucose in liver may impair several cellular processes thus leading to injury.
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