Abstract
The insulin receptor substrate-2/phosphoinositide 3-kinase (PI3K) pathway plays a critical role in the regulation of beta-cell mass and function, demonstrated both in vitro and in vivo. The serine threonine kinase Akt is one of the promising downstream molecules of this pathway that has been identified as a potential target to regulate function and induce proliferation and survival of beta cells. Here we summarize some of the molecular mechanisms, downstream signalling pathways and critical components involved in the regulation of beta-cell mass and function by Akt.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Apoptosis
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Cell Proliferation
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Diabetes Mellitus, Type 2 / metabolism*
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Humans
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Insulin-Secreting Cells / enzymology
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Insulin-Secreting Cells / physiology*
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Mice
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PTEN Phosphohydrolase / metabolism
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Phosphatidylinositol 3-Kinases / metabolism*
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Protein Isoforms / metabolism
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Protein Serine-Threonine Kinases / metabolism
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Proto-Oncogene Proteins c-akt / metabolism*
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Rats
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Signal Transduction / physiology*
Substances
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Protein Isoforms
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Protein Serine-Threonine Kinases
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Proto-Oncogene Proteins c-akt
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PTEN Phosphohydrolase