Acute exposure to rosiglitazone does not affect glucose transport in intact human skeletal muscle.

[1]  H. Koistinen,et al.  Globular adiponectin stimulates glucose transport in type 2 diabetic muscle , 2008, Diabetes/metabolism research and reviews.

[2]  S. Knudsen,et al.  Pioglitazone Enhances Mitochondrial Biogenesis and Ribosomal Protein Biosynthesis in Skeletal Muscle in Polycystic Ovary Syndrome , 2008, PloS one.

[3]  Peter Tontonoz,et al.  Fat and beyond: the diverse biology of PPARgamma. , 2008, Annual review of biochemistry.

[4]  G. McVeigh,et al.  Thiazolidinediones: effects on insulin resistance and the cardiovascular system , 2008, British journal of pharmacology.

[5]  K. Sugimura,et al.  Effects of pioglitazone and metformin on intracellular lipid content in liver and skeletal muscle of individuals with type 2 diabetes mellitus. , 2007, Metabolism: clinical and experimental.

[6]  D. Hardie,et al.  AMP-activated/SNF1 protein kinases: conserved guardians of cellular energy , 2007, Nature Reviews Molecular Cell Biology.

[7]  J. Zierath,et al.  AMP-activated protein kinase signaling in metabolic regulation. , 2006, The Journal of clinical investigation.

[8]  N. LeBrasseur,et al.  Thiazolidinediones can rapidly activate AMP-activated protein kinase in mammalian tissues. , 2006, American journal of physiology. Endocrinology and metabolism.

[9]  H. Koistinen,et al.  Insulin Signaling and Glucose Transport in Skeletal Muscle From First-Degree Relatives of Type 2 Diabetic Patients , 2006, Diabetes.

[10]  S. Mudaliar,et al.  Impaired fatty acid metabolism in type 2 diabetic skeletal muscle cells is reversed by PPARgamma agonists. , 2005, American journal of physiology. Endocrinology and metabolism.

[11]  A. Rudich,et al.  Troglitazone causes acute mitochondrial membrane depolarisation and an AMPK-mediated increase in glucose phosphorylation in muscle cells , 2005, Diabetologia.

[12]  A. Häkkinen,et al.  Effects of rosiglitazone and metformin on liver fat content, hepatic insulin resistance, insulin clearance, and gene expression in adipose tissue in patients with type 2 diabetes. , 2004, Diabetes.

[13]  G. Cooney,et al.  Direct demonstration of lipid sequestration as a mechanism by which rosiglitazone prevents fatty-acid-induced insulin resistance in the rat: comparison with metformin , 2004, Diabetologia.

[14]  M. Roden,et al.  Thiazolidinediones, like metformin, inhibit respiratory complex I: a common mechanism contributing to their antidiabetic actions? , 2004, Diabetes.

[15]  B. Spiegelman,et al.  Muscle-specific PPARgamma-deficient mice develop increased adiposity and insulin resistance but respond to thiazolidinediones. , 2003, The Journal of clinical investigation.

[16]  Y. Miyazaki,et al.  Rosiglitazone improves downstream insulin receptor signaling in type 2 diabetic patients. , 2003, Diabetes.

[17]  H. Koistinen,et al.  5-amino-imidazole carboxamide riboside increases glucose transport and cell-surface GLUT4 content in skeletal muscle from subjects with type 2 diabetes. , 2003, Diabetes.

[18]  D. Doddrell,et al.  Effect of rosiglitazone on insulin sensitivity and body composition in type 2 diabetic patients [corrected]. , 2002, Obesity research.

[19]  David Carling,et al.  The Anti-diabetic Drugs Rosiglitazone and Metformin Stimulate AMP-activated Protein Kinase through Distinct Signaling Pathways* , 2002, The Journal of Biological Chemistry.

[20]  Vincent Lebon,et al.  The effects of rosiglitazone on insulin sensitivity, lipolysis, and hepatic and skeletal muscle triglyceride content in patients with type 2 diabetes. , 2002, Diabetes.

[21]  S. Mudaliar,et al.  Troglitazone but not metformin restores insulin-stimulated phosphoinositide 3-kinase activity and increases p110beta protein levels in skeletal muscle of type 2 diabetic subjects. , 2002, Diabetes.

[22]  Y. Terauchi,et al.  The Mechanisms by Which Both Heterozygous Peroxisome Proliferator-activated Receptor γ (PPARγ) Deficiency and PPARγ Agonist Improve Insulin Resistance* , 2001, The Journal of Biological Chemistry.

[23]  M. Roden,et al.  Direct thiazolidinedione action on isolated rat skeletal muscle fuel handling is independent of peroxisome proliferator-activated receptor-gamma-mediated changes in gene expression. , 2001, Diabetes.

[24]  M. Prentki,et al.  Activation of Malonyl-CoA Decarboxylase in Rat Skeletal Muscle by Contraction and the AMP-activated Protein Kinase Activator 5-Aminoimidazole-4-carboxamide-1-β-d-ribofuranoside* , 2000, The Journal of Biological Chemistry.

[25]  J. Nolan,et al.  Rosiglitazone taken once daily provides effective glycaemic control in patients with Type 2 diabetes mellitus , 2000, Diabetic medicine : a journal of the British Diabetic Association.

[26]  P. Raskin,et al.  Rosiglitazone short-term monotherapy lowers fasting and post-prandial glucose in patients with Type II diabetes , 2000, Diabetologia.

[27]  D. Hardie,et al.  AMP-activated protein kinase, a metabolic master switch: possible roles in Type 2 diabetes. , 1999, American journal of physiology. Endocrinology and metabolism.

[28]  P. Raskin,et al.  Effect of troglitazone in insulin-treated patients with type II diabetes mellitus. Troglitazone and Exogenous Insulin Study Group. , 1998, The New England journal of medicine.

[29]  C. Burant,et al.  Troglitazone action is independent of adipose tissue. , 1997, The Journal of clinical investigation.

[30]  J. Auwerx,et al.  Tissue Distribution and Quantification of the Expression of mRNAs of Peroxisome Proliferator–Activated Receptors and Liver X Receptor-α in Humans: No Alteration in Adipose Tissue of Obese and NIDDM Patients , 1997, Diabetes.

[31]  M. Jimenez-Linan,et al.  Peroxisome proliferator-activated receptor gene expression in human tissues. Effects of obesity, weight loss, and regulation by insulin and glucocorticoids. , 1997, The Journal of clinical investigation.

[32]  B. Ludvik,et al.  Improvement in glucose tolerance and insulin resistance in obese subjects treated with troglitazone. , 1994, The New England journal of medicine.

[33]  E. Ravussin,et al.  Insulin resistance and insulin secretory dysfunction as precursors of non-insulin-dependent diabetes mellitus. Prospective studies of Pima Indians. , 1993, The New England journal of medicine.

[34]  R. DeFronzo.  The Triumvirate: β-Cell, Muscle, Liver: A Collusion Responsible for NIDDM , 1988, Diabetes.

[35]  R. Levy,et al.  Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. , 1972, Clinical chemistry.

[36]  J. Berger,et al.  Role of Skeletal Muscle in Thiazolidinedione Insulin Sensitizer ( PPAR g Agonist ) Action , 1998 .