The defining characteristic of diabetes is its failure to properly maintain blood glucose levels. Normally, the elevated glucose concentration that occurs after eating induces the release of the hormone insulin from pancreatic beta cells. Cells expressing the insulin receptor can bind insulin and respond to the signal, thereby maintaining glucose homeostasis through changes in gene expression patterns and cellular metabolism. Insulin-induced effects include enhanced glucose uptake and glycogen synthesis, decreased lipolysis, stimulated fatty acid synthesis, and enhanced protein translation. Unfortunately, what is known about the activity between insulin binding outside of the cell and metabolic changes inside the cell is limited.
During the American Diabetes Association national conference this year in Philadelphia, scientists gathered to discuss recent advances in this field at a session on positive and negative elements in signal transduction. When all was said and done, some puzzle pieces were added, but questions remain.
Because diabetes essentially results...
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