Guest guest Posted January 8, 2001 Report Share Posted January 8, 2001 Here's a forward from LC-D list/Ron that I thought this group might appreciate...Vicki << The term burnout is usually taken to mean death of beta cells. The Moran study and quite a few others that a search for Exhaustion AND Beta will return in Pubmed, state that chemical and genetic alterations take place. They are somewhat reversible, and barring beta cell resurrection, that suggests the cells were not dead. The Moran paper and another follow up paper that is much more recent, show that high glucose levels are a cause of damage. The literature suggests that this is glycation damage; the more recent paper showed that reversibility lessens as time of immersion in high glucose levels increases. That is precisely what production of advanced glycation end products would lead us to expect. If they are correct about the cause, that means that peaks do not matter much but long term average sugar levels matter plenty. The other beta cell damage causes I see here and there in journals are free radical damage and damage from triglycerides. Do a search on lipotoxicity at PubMed (aka Medline) and the triglyceride story will appear. The above is precisely why I was brought to the conclusion that aggressive antioxidant application, aggressive lipid management (which of course is critical to lowering risk of arterial disease too), and tight control of blood sugar were a package deal. There is no study I know of that shows that these measures will arrest the progression of beta cell decline. However, lacking such studies, it seems logical to hypothesize that if you address know sources of damage that may reduce of eliminate the damage. Time will tell. Ron Quote Link to comment Share on other sites More sharing options...
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