In Vivo Administration of Glucosamine Inhibited Phosphatidylinositol 3-Kinase Activity without Affecting Tyrosine Phosphorylation of the Insulin Receptor or Insulin Receptor Substrate in Rat Adipocytes
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概要
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We examined insulin signaling in rat epididymal adipocytes which developed insulinresistance by the in vivo infusion of glucosamine. Insulin-stimulated 2-deoxyglucoseuptake into the adipocytes isolated from rats which were infused glucosamine for 4hours was diminished by 26%. To analyze insulin signaling in adipocytes, the epididymalfat tissues were harvested 5 minutes after insulin administration (10U/kg), which wasadministered immediately after glucosamine infusion. Glucosamine had no effect on theinsulin-stimulated tyrosine phosphorylation of the insulin receptor and insulin receptorsubstrate (IRS)-1. Glucosamine infusion decreased insulin-stimulated phosphatidylinositol(PI) 3-kinase activity by 66%. Glucosamine infusion also inhibited insulin-stimulated PI3-kinase activity associated with IRS-1, 2, 3 by 30%, 43%, and 44%, respectively. Therewas no difference in the association of the 85kDa subunit of PI 3-kinase with the IRS-1and IRS-2 protein. PI 3-kinase activity in adipocytes from rats treated with glucosaminethat were administered platelet derived growth factor (3μg/kg) for 5 minutes was alsoreduced by 39%. When we measured the kinase activity of protein kinase C (PKC) λ,which is the downstream effector of PI 3-kinase in isolated adipocytes, we found thatglucosamine inhibited insulin stimulated PKCλ kinase activity by 33%. These resultssuggest that glucosamine infusion contributes to the development of insulin resistance bymainly modulating the PI 3-kinase molecules.
- 神戸大学の論文
著者
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Kasuga Masato
神戸大学医学系研究科
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Kasuga Masato
Department Of Clinical Molecular Medicine Division Of Diabetes Digestive And Kidney Diseases
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Kasuga M
Kobe Univ. Graduate School Of Medicine
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Miki Takeshi
神戸大学医学系研究科
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Sakaue Motoyoshi
神戸大学医学系研究科
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