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QUOTE: ...The Warwick research team, led by Dr Antonio Ceriello, have now proven that the damage seems to be done in a process called glycation when early on in a period of high glucose levels glucose sugar molecules are able to bind to proteins in the mitochondria of cells (the parts of cells governing the production and regulation of energy). This persists even if glucose levels later fall to normal. This inhibits and distorts the mitochondria’s normal function and results in an overabundance of the production of free radicals (or Reactive Oxygen Species �?ROS) which cause oxidation and thus continued diabetic complications.
The Warwick Medical School researchers proved their hypothesis by taking tissue and exposing it to 2 weeks of high levels of glucose, followed by one week of normal glucose �?however for half the tissue they also applied several antioxidants at the end of the two weeks of high glucose. The tissue without antioxidants levels of glucose stress remained high but where antioxidants had been applied there was a dramatic fall in the incidence of free radicals and there was also a significant drop in 5 of the 6 key markers for high glucose stress... Dr Ceriello’s paper "Reactive oxygen species mediate a cellular ‘memory�?of high glucose stress signaling" has just been published in Diabetologia DOI 10.1007/s00125-007-0684-2. The second paper, about to be published in Diabetes Care, is entitled "Antioxidants and Free Radicals, Endothelial Dysfunction, Oxidative and Nitrosative Stress covers his work on the AT-1 receptor blocker Telmisartan. UNQUOTE.
Source: http://www.sciencedaily.com/releases/2007/06/070628162254.htm |
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