Application | Comment | Organism |
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medicine | in patients with polycystic ovary syndrome, reduced insulin-mediated glucose disposal is associated with a lower insulin-stimulated glycogen synthase activity, explained by absent insulin-mediated dephosphorylation of glycogen synthase at the NH2-terminal sites 2 + 2a, whereas dephosphorylation at the COOH-terminal sites 3a + 3b is intact in polycystic ovary syndrome subjects. Insulin activation of glycogen synthase is dependent on dephosphorylation of sites 3a + 3b in women with polycystic ovary syndrome. No significant abnormalities in glycogen synthaseK-3 or -3 are found. Pioglitazone treatment improves insulin-stimulated glucose metabolism and glycogen synthase activity in polycystic ovary syndrome and restores the ability of insulin to dephosphorylate glycogen synthase at sites 2 and 2a | Homo sapiens |
Organism | UniProt | Comment | Textmining |
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Homo sapiens | - |
patients with polycystic ovary syndrome | - |
Source Tissue | Comment | Organism | Textmining |
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skeletal muscle | - |
Homo sapiens | - |