The Experts below are selected from a list of 33795 Experts worldwide ranked by ideXlab platform
Lorraine A Fitzpatrick - One of the best experts on this subject based on the ideXlab platform.
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pathophysiology of bone loss in patients receiving anticonvulsant therapy
Epilepsy & Behavior, 2004Co-Authors: Lorraine A FitzpatrickAbstract:Many studies have shown that patients taking antiepileptic drugs (AEDs) are at increased risk for metabolic bone disease and low bone mineral density. Although early reports of bone disease in patients with epilepsy often involved institutionalized patients, who may be at risk because of lack of physical activity, reduced sunlight exposure, and poor nutrition, low bone density has also been reported in well-nourished, ambulatory outpatients with epilepsy. Traditionally, attention to the problem of AED-induced bone loss has been focused on those drugs that induce the hepatic cytochrome P450 enzyme system, thereby increasing the metabolism of vitamin D. However, the mechanisms of AED-induced bone loss appear to be multiple, and all types of AEDs are potentially implicated. Besides hepatic enzyme induction, mechanisms may include direct effects of AEDs on bone cells, resistance to parathyroid Hormone, Inhibition of calcitonin secretion, and impaired calcium absorption. An understanding of bone biology and the pathophysiology of bone loss can aid in the identification and monitoring of patients at risk and in the planning of appropriate prophylactic and therapeutic measures, by which most of the morbidity associated with AED-induced bone loss can be prevented.
Fumihiko Hakuno - One of the best experts on this subject based on the ideXlab platform.
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growth Hormone Inhibition of glucose uptake in adipocytes occurs without affecting glut4 translocation through an insulin receptor substrate 2 phosphatidylinositol 3 kinase dependent pathway
Journal of Biological Chemistry, 2009Co-Authors: Naoko Sasakisuzuki, Kiyoshi Arai, Tomomi Ogata, Kouhei Kasahara, Hideyuki Sakoda, Kazuhiro Chida, Tomoichiro Asano, Jeffrey E Pessin, Fumihiko HakunoAbstract:Growth Hormone (GH) pretreatment of 3T3-L1 adipocytes resulted in a concentration- and time-dependent Inhibition of insulin-stimulated glucose uptake. Surprisingly, this occurred without significant effect on insulin-stimulated glucose transporter (GLUT) 4 translocation or fusion with the plasma membrane. In parallel, the inhibitory actions of chronic GH pretreatment also impaired insulin-dependent activation of phosphatidylinositol (PI) 3-kinase bound to insulin receptor substrate (IRS)-2 but not to IRS-1. In addition, insulin-stimulated Akt phosphorylation was inhibited by GH pretreatment. In contrast, overexpression of IRS-2 or expression of a constitutively active Akt mutant prevented the GH-induced insulin resistance of glucose uptake. Moreover, small interfering RNA-mediated IRS-2 knockdown also inhibited insulin-stimulated Akt activation and glucose uptake without affecting GLUT4 translocation and plasma membrane fusion. Together, these data support a model in which chronic GH stimulation inhibits insulin-dependent activation of phosphatidylinositol 3-kinase through a specific interaction of phosphatidylinositol 3-kinase bound to IRS-2. This Inhibition leads to suppression of Akt activation coupled to glucose transport activity but not translocation or plasma membrane fusion of GLUT4.
Tomoichiro Asano - One of the best experts on this subject based on the ideXlab platform.
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growth Hormone Inhibition of glucose uptake in adipocytes occurs without affecting glut4 translocation through an insulin receptor substrate 2 phosphatidylinositol 3 kinase dependent pathway
Journal of Biological Chemistry, 2009Co-Authors: Naoko Sasakisuzuki, Kiyoshi Arai, Tomomi Ogata, Kouhei Kasahara, Hideyuki Sakoda, Kazuhiro Chida, Tomoichiro Asano, Jeffrey E Pessin, Fumihiko HakunoAbstract:Growth Hormone (GH) pretreatment of 3T3-L1 adipocytes resulted in a concentration- and time-dependent Inhibition of insulin-stimulated glucose uptake. Surprisingly, this occurred without significant effect on insulin-stimulated glucose transporter (GLUT) 4 translocation or fusion with the plasma membrane. In parallel, the inhibitory actions of chronic GH pretreatment also impaired insulin-dependent activation of phosphatidylinositol (PI) 3-kinase bound to insulin receptor substrate (IRS)-2 but not to IRS-1. In addition, insulin-stimulated Akt phosphorylation was inhibited by GH pretreatment. In contrast, overexpression of IRS-2 or expression of a constitutively active Akt mutant prevented the GH-induced insulin resistance of glucose uptake. Moreover, small interfering RNA-mediated IRS-2 knockdown also inhibited insulin-stimulated Akt activation and glucose uptake without affecting GLUT4 translocation and plasma membrane fusion. Together, these data support a model in which chronic GH stimulation inhibits insulin-dependent activation of phosphatidylinositol 3-kinase through a specific interaction of phosphatidylinositol 3-kinase bound to IRS-2. This Inhibition leads to suppression of Akt activation coupled to glucose transport activity but not translocation or plasma membrane fusion of GLUT4.
Stefano Leone - One of the best experts on this subject based on the ideXlab platform.
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thyroid Hormone Inhibition in l6 myoblasts of igf i mediated glucose uptake and proliferation new roles for integrin αvβ3
American Journal of Physiology-cell Physiology, 2014Co-Authors: Sandra Incerpi, Meng Ti Hsieh, Hung Yun Lin, Guei Yun Cheng, Paolo De Vito, Anna Maria Fiore, Rafay Ahmed, Rosanna Salvia, Elena Candelotti, Stefano LeoneAbstract:Thyroid Hormones l-thyroxine (T4) and 3,3′,5-triiodo-l-thyronine (T3) have been shown to initiate short- and long-term effects via a plasma membrane receptor site located on integrin αvβ3. Also ins...
Naoko Sasakisuzuki - One of the best experts on this subject based on the ideXlab platform.
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growth Hormone Inhibition of glucose uptake in adipocytes occurs without affecting glut4 translocation through an insulin receptor substrate 2 phosphatidylinositol 3 kinase dependent pathway
Journal of Biological Chemistry, 2009Co-Authors: Naoko Sasakisuzuki, Kiyoshi Arai, Tomomi Ogata, Kouhei Kasahara, Hideyuki Sakoda, Kazuhiro Chida, Tomoichiro Asano, Jeffrey E Pessin, Fumihiko HakunoAbstract:Growth Hormone (GH) pretreatment of 3T3-L1 adipocytes resulted in a concentration- and time-dependent Inhibition of insulin-stimulated glucose uptake. Surprisingly, this occurred without significant effect on insulin-stimulated glucose transporter (GLUT) 4 translocation or fusion with the plasma membrane. In parallel, the inhibitory actions of chronic GH pretreatment also impaired insulin-dependent activation of phosphatidylinositol (PI) 3-kinase bound to insulin receptor substrate (IRS)-2 but not to IRS-1. In addition, insulin-stimulated Akt phosphorylation was inhibited by GH pretreatment. In contrast, overexpression of IRS-2 or expression of a constitutively active Akt mutant prevented the GH-induced insulin resistance of glucose uptake. Moreover, small interfering RNA-mediated IRS-2 knockdown also inhibited insulin-stimulated Akt activation and glucose uptake without affecting GLUT4 translocation and plasma membrane fusion. Together, these data support a model in which chronic GH stimulation inhibits insulin-dependent activation of phosphatidylinositol 3-kinase through a specific interaction of phosphatidylinositol 3-kinase bound to IRS-2. This Inhibition leads to suppression of Akt activation coupled to glucose transport activity but not translocation or plasma membrane fusion of GLUT4.