Alan S wrote:

>>Catherine E. Gleason, Michael Gonzalez, Jamie S. Harmon, and R. Paul
>>Robertson. Determinants of glucose toxicity and its reversibility in
>>pancreatic islet Beta-cell line, HIT-T15. Am J Physiol Endocrinol Metab
>>279: E997-E1002, 2000
>>
>>http://ajpendo.physiology.org/cgi/co...act/279/5/E997
>>
>
>
> That's a really interesting paper. It's specifically
> interested in beta-cell damage and recovery, not other
> damage that may occur to the body from spikes.
(snipped)

> "In summary, these findings indicate that glucose
> toxicity of the b-cell is a continuous rather than a
> threshold function of glucose concentration and that
> the shorter the period of antecedent glucose toxicity,
> the greater the degree of recovery.
(snipped)
> On the other hand, a spectrum of pathophysiological
> changes may occur with more prolonged exposure of
> the b-cell to supraphysiological glucose concentrations.
>
(snipped)
>
> In this context, it seems likely that early, effective
> management by diet and drugs of hyperglycemia in type 2
> diabetes is an important aspect of preserving residual
> b-cell function. The same argument for meticulous glycemic
> control can be made after pancreas or islet
> transplantation."
>

TABLE 1 Literature supporting chronic oxidative stress as a mechanism
for glucose toxicity of the ß-cell -
http://diabetes.diabetesjournals.org...ll/52/3/581/T1

Treating Postprandial Hyperglycemia Does Not Appear to Delay Progression
of Early Type 2 Diabetes -
http://care.diabetesjournals.org/cgi...full/29/9/2095


Frank