نتایج جستجو برای: glucose uptake

تعداد نتایج: 303044  

2005
Jin Gyoon Park Sabina Semiz John Holik Shraddha Patel

Glucose transporter 4 (GLUT4) moves from perinuclear storage regions to the plasma membrane in response to insulin and facilitates glucose uptake. This MQP examined the roles of three proteins (GAPDH, PGK, and PGAM) in glucose uptake and GLUT4 trafficking in 3T3-L1 adipocytes by performing glucose uptake assays on adipocytes in which these proteins were selectively knocked down using RNAi. GLUT...

Journal: :Diabetes 2002
Bronwyn A Kingwell Melissa Formosa Michael Muhlmann Scott J Bradley Glenn K McConell

Nitric oxide (NO) synthase inhibition reduces leg glucose uptake during cycling without reducing leg blood flow (LBF) in young, healthy individuals. This study sought to determine the role of NO in glucose uptake during exercise in individuals with type 2 diabetes. Nine men with type 2 diabetes and nine control subjects matched for age, sex, peak pulmonary oxygen uptake (VO(2) peak), and weight...

Journal: :Diabetes 2002
Carol Huang Romel Somwar Nish Patel Wenyan Niu Dóra Török Amira Klip

Hyperglycemia and hyperinsulinemia are cardinal features of acquired insulin resistance. In adipose cell cultures, high glucose and insulin cause insulin resistance of glucose uptake, but because of altered GLUT4 expression and contribution of GLUT1 to glucose uptake, the basis of insulin resistance could not be ascertained. Here we show that GLUT4 determines glucose uptake in L6 myotubes stabl...

2015
Giovanni Messina Filomena Palmieri Vincenzo Monda Antonietta Messina Carmine Dalia Andrea Viggiano Domenico Tafuri Fiorenzo Moscatelli Anna Valenzano Giuseppe Cibelli Sergio Chieffi Marcellino Monda

Glucose uptake in skeletal muscle is dependent on the translocation of GLUT4 glucose transporters to the plasma membrane. The most important stimulators of glucose transport in skeletal muscle are insulin and exercise. Glucose uptake in skeletal muscle during exercise induces acceleration of many processes compared to the resting state. The scientific literature does not underline the role play...

Journal: :American journal of physiology. Cell physiology 2008
Carolyn L Buller Robert D Loberg Ming-Hui Fan Qihong Zhu James L Park Eileen Vesely Ken Inoki Kun-Liang Guan Frank C Brosius

Glucose transport is a highly regulated process and is dependent on a variety of signaling events. Glycogen synthase kinase-3 (GSK-3) has been implicated in various aspects of the regulation of glucose transport, but the mechanisms by which GSK-3 activity affects glucose uptake have not been well defined. We report that basal glycogen synthase kinase-3 (GSK-3) activity regulates glucose transpo...

Journal: :Microbiology 2007
Thomas R Jørgensen Patricia A vanKuyk Bjarne R Poulsen George J G Ruijter Jaap Visser Jens J L Iversen

This is a study of high-affinity glucose uptake in Aspergillus niger and the effect of disruption of a high-affinity monosaccharide-transporter gene, mstA. The substrate saturation constant (K(s)) of a reference strain was about 15 microM in glucose-limited chemostat culture. Disruption of mstA resulted in a two- to fivefold reduction in affinity for glucose and led to expression of a low-affin...

Journal: :Journal of pharmacological sciences 2011
Shuichiro Yano Saori Morino-Koga Tatsuya Kondo Mary Ann Suico Tomoaki Koga Yuichiro Shimauchi Shingo Matsuyama Tsuyoshi Shuto Takashi Sato Eiichi Araki Hirofumi Kai

Activation of Akt by insulin is transmitted via phosphatidylinositol-3-OH kinase (PI-3K) and enhances glucose uptake. The PI-3K/Akt signaling is diminished in insulin resistance. Thus, approaches that activate PI-3K/Akt signaling leading to improved glucose uptake may ameliorate hyperglycemia. Here we showed that low-intensity electrical current or mild electrical stimulation (MES) activated th...

Journal: :The Journal of clinical investigation 2001
J K Kim A Zisman J J Fillmore O D Peroni K Kotani P Perret H Zong J Dong C R Kahn B B Kahn G I Shulman

Using cre/loxP gene targeting, transgenic mice with muscle-specific inactivation of the GLUT4 gene (muscle GLUT4 KO) were generated and shown to develop a diabetes phenotype. To determine the mechanism, we examined insulin-stimulated glucose uptake and metabolism during hyperinsulinemic-euglycemic clamp in control and muscle GLUT4 KO mice before and after development of diabetes. Insulin-stimul...

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