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AMP-activated protein kinase (AMPK) regulates glucose, lipid and protein metabolism in mammalian cells. In certain tissues, AMPK activation may have anti-obesity and anti-diabetic effects, which are thought to be responsible for the insulin-sensitizing properties of drugs such as metformin. We investigated the role of AMPK in pancreatic beta-cell function using pharmacological and hormonal approaches. The compound alpha-lipoic acid (alpha-LA) was shown to be a potent AMPK-activating compound in isolated islets and MIN6 beta-cells. Treatment with alpha-LA caused an inhibition of insulin secretion and cell growth, possibly owing to AMPK activation and pro-oxidant properties. The adipose-derived hormone adiponectin, which regulates AMPK in muscle and liver, did not induce changes in this enzyme in MIN6 cells. Subsequent cloning and expression of the adiponectin receptors neither facilitated AMPK activity nor demonstrated an interaction with its ligand. These studies show that alpha-LA, but not adiponectin, regulates AMPK and insulin secretion in beta-cells.
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Pharmacological and hormonal regulation of AMP-activated protein kinase in the pancreatic [beta]-cell.
2005
in English
0494075058 9780494075050
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Source: Masters Abstracts International, Volume: 44-02, page: 0744.
Thesis (M.Sc.)--University of Toronto, 2005.
Electronic version licensed for access by U. of T. users.
GERSTEIN MICROTEXT copy on microfiche (2 microfiches).
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