Abstract
Pancreatic β-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 β-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 β-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 β-cell genes, particularly the insulin gene itself. More controversially, this insulin feedback has also been suggested to either terminate or enhance insulin secretion events.
| Original language | English |
|---|---|
| Journal | American Journal of Physiology - Endocrinology and Metabolism |
| Volume | 283 |
| Issue number | 6 46-6 |
| State | Published - Dec 1 2002 |
| Externally published | Yes |
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Keywords
- Inositol lipids
- Inositol polyphosphates
- Insulin receptor
- Insulin secretion
- Pancreatic β-cell
ASJC Scopus subject areas
- Physiology
- Endocrinology
- Biochemistry
Cite this
Phosphorylated inositol compounds in β-cell stimulus-response coupling. / Barker, Christopher J.; Leibiger, Ingo B.; Leibiger, Barbara; Berggren, Per Olof.
In: American Journal of Physiology - Endocrinology and Metabolism, Vol. 283, No. 6 46-6, 01.12.2002.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Phosphorylated inositol compounds in β-cell stimulus-response coupling
AU - Barker, Christopher J.
AU - Leibiger, Ingo B.
AU - Leibiger, Barbara
AU - Berggren, Per Olof
PY - 2002/12/1
Y1 - 2002/12/1
N2 - Pancreatic β-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 β-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 β-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 β-cell genes, particularly the insulin gene itself. More controversially, this insulin feedback has also been suggested to either terminate or enhance insulin secretion events.
AB - Pancreatic β-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 β-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 β-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 β-cell genes, particularly the insulin gene itself. More controversially, this insulin feedback has also been suggested to either terminate or enhance insulin secretion events.
KW - Inositol lipids
KW - Inositol polyphosphates
KW - Insulin receptor
KW - Insulin secretion
KW - Pancreatic β-cell
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M3 - Article
C2 - 12424101
AN - SCOPUS:0036888993
VL - 283
JO - American Journal of Physiology - Cell Physiology
JF - American Journal of Physiology - Cell Physiology
SN - 0363-6143
IS - 6 46-6
ER -