The β-cell glucose toxicity hypothesis: attractive but difficult to prove

β cells in the hyperglycemic environment of diabetes have marked changes in phenotype and function that are largely reversible if glucose levels can be returned to normal. A leading hypothesis is that these changes are caused by the elevated glucose levels leading to the concept of glucose toxicity . Support for the glucose toxicity hypothesis is largely circumstantial, but little progress has been made in defining the responsible mechanisms. Then questions emerge that are difficult to answer. In the very earliest stages of diabetes development, there is a dramatic loss of glucose-induced firs t-phase insulin release (FPIR) with only trivial elevations of blood glucose levels.
Source: Metabolism - Clinical and Experimental - Category: Biomedical Science Authors: Source Type: research