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-cell
stimulus-response coupling
Department of Molecular Medicine, The Rolf Luft Center for Diabetes Research, Karolinska Institutet, S-171 76 Stockholm, Sweden
Pancreatic
-cell function is essential for the regulation of glucose
homeostasis in humans, and its impairment leads to the development of
type 2 diabetes. Inputs from glucose and cell surface receptors act
together to initiate the -cell stimulus-response coupling that
ultimately leads to the release of insulin. Phosphorylated inositol
compounds have recently emerged as key players at all levels of the
stimulus-secretion coupling process. In this current review, we seek to
highlight recent advances in -cell phosphoinositide research by
dividing our examination into two sections. The first involves the
events that lead to insulin secretion. This includes both new roles for
inositol polyphosphates, particularly inositol hexakisphosphate, and
both conventional and 3-phosphorylated inositol lipids. In the second
section, we deal with the more novel concept of the autocrine role of
insulin. Here, released insulin initiates signal transduction cascades,
principally through the activity of phosphatidylinositol 3-kinase. This
new round of signal transduction has been established to activate key
-cell genes, particularly the insulin gene itself. More
controversially, this insulin feedback has also been suggested to
either terminate or enhance insulin secretion events.
inositol polyphosphates; inositol lipids; insulin receptor; insulin
secretion; pancreatic -cell
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