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Health News Archive 233 - Diabetes
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Benfotiamine Alleviates Oxidative Stress in Brains of Diabetic Rodents

Benfotiamine, a derivative of thiamine, reduces the free radical caused oxidative damage that occurs in the brains of diabetic mice, according to a study published February 2006 in Neuroscience Letters.

Diabetes mellitus leads to thiamine deficiency and multiple organ damage including diabetic neuropathy. This study was designed to examine the effect of benfotiamine, a lipophilic derivative of thiamine, on streptozotocin (STZ)-induced cerebral oxidative stress. Benfotiamine alleviated diabetes-induced cerebral oxidative stress without affecting levels of AGE, protein carbonyl, tissue factor and TNF-alpha. Collectively, our results indicated benfotiamine may antagonize diabetes-induced cerebral oxidative stress through a mechanism unrelated to AGE, tissue factor and TNF-alpha.

Male mice were made diabetic by the injection of a substance called streptozotocin. Control and diabetic mice received benfotiamine (100 mg/kg per day administered within the lining of the abdominal cavity) for 14 days. The researchers then evaluated oxidative stress and protein damage in the animals. Pro-oxidative or pro-inflammatory factors including advanced glycation end-products (AGEs) and tissue factor and tumor necrosis factor-alpha (TNF-alpha) were also evaluated. AGEs are toxic end products that occur when there are ongoing, high levels of sugars and hormones in the body. TNF-Alpha is a protein produced by white blood cells that helps regulate the immune response.

Four weeks after diabetes was induced in the animals, the mice suffered from hyperglycemia, enhanced cerebral oxidative stress and elevated TNF-alpha and AGE levels. In the diabetic animals treated with benfotiamine, however, the diabetes-induced cerebral oxidative stress was significantly reduced without affecting levels of AGEs or TNF-alpha.

The researchers concluded that the results indicated benfotiamine may reduce diabetes-induced cerebral oxidative stress through a mechanism unrelated to stopping the formation of AGEs and TNF-alpha.

Reference: Wu S, Ren J. Benfotiamine alleviates diabetes-induced cerebral oxidative damage independent of advanced glycation end-product, tissue factor and TNF-alpha. Neurosci Lett. 2006 Feb 13;394(2):158-62. Epub 2005 Oct 28.