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Genomes and Genes | J T BrozinickSummaryAffiliation: Eli Lilly and Company Country: USA Publications
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Publications
"Actin"g on GLUT4: membrane & cytoskeletal components of insulin actionJoseph T Brozinick
Eli Lilly and Company, Lilly Corporate Center, Indianapolis, IN 46285, USA
Curr Diabetes Rev 3:111-22. 2007..The discussion will visit recent cell culture, whole animal, and human data highlighting membrane and cytoskeletal aspects of insulin resistance...- Disruption of cortical actin in skeletal muscle demonstrates an essential role of the cytoskeleton in glucose transporter 4 translocation in insulin-sensitive tissuesJoseph T Brozinick
Eli Lilly and Company, Indianapolis, Indiana 46285, USA
J Biol Chem 279:40699-706. 2004..Furthermore, these findings support a distal actin-based role for N-WASP in insulin action in vivo... 
Defective signaling through Akt-2 and -3 but not Akt-1 in insulin-resistant human skeletal muscle: potential role in insulin resistanceJoseph T Brozinick
Eli Lilly and Company, Lilly Corporate Center, Indianapolis, Indiana, USA
Diabetes 52:935-41. 2003..Additionally, these data also show that different upstream or downstream signals may regulate the activity of the various Akt isoforms...- 1-[N, O-bis-(5-isoquinolinesulphonyl)-N-methyl-L-tyrosyl]-4- phenylpiperazine (KN-62), an inhibitor of calcium-dependent camodulin protein kinase II, inhibits both insulin- and hypoxia-stimulated glucose transport in skeletal muscleJ T Brozinick
Experimental Diabetes, Metabolism and Nutrition Section, DB NIDDK National Institutes of Health, Bethesda, MD 20892, USA
Biochem J 339:533-40. 1999..The results of the present study suggest that CAMKII might have a distinct role in insulin- and hypoxia-stimulated glucose transport, possibly in the vesicular trafficking of GLUT4... - Insulin, but not contraction, activates Akt/PKB in isolated rat skeletal muscleJ T Brozinick
Howard Hughes Medical Institute, Department of Medicine and The Cox Institute, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104 6148, USA
J Biol Chem 273:14679-82. 1998..These data provide further evidence that two distinct pathways exist for the stimulation of glucose transport in mammalian skeletal muscle... - GLUT4 overexpression in db/db mice dose-dependently ameliorates diabetes but is not a lifelong cureJ T Brozinick
Experimental Diabetes, Metabolism and Nutrition Section, DB NIDDK, National Institutes of Health, Bethesda, Maryland, USA
Diabetes 50:593-600. 2001..In summary, despite an impairment in whole-body glucose tolerance, skeletal muscle of the old transgenic GLUT4 db/db mice is still insulin responsive in vitro and in vivo... - Regulation of cell surface GLUT4 in skeletal muscle of transgenic miceJ T Brozinick
Experimental Diabetes, Metabolism and Nutrition Section, DB NIDDK National Institutes of Health, Bethesda, MD 20892, USA
Biochem J 321:75-81. 1997.... - Transient enhancement of GLUT-4 levels in rat epitrochlearis muscle after exercise trainingT H Reynolds
Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA
J Appl Physiol 88:2240-5. 2000..We believe that the transient enhancement in GLUT-4 protein after exercise training is due to a short GLUT-4 half-life, a process that is primarily regulated by pretranslational mechanisms... - A role for AMP-activated protein kinase in contraction- and hypoxia-regulated glucose transport in skeletal muscleJ Mu
Howard Hughes Medical Institute, The Cox Institute, The Department of Medicine, University of Pennsylvania Medical School, Philadelphia, PA 19104, USA
Mol Cell 7:1085-94. 2001..These data indicate that AMPK transmits a portion of the signal by which muscle contraction increases glucose uptake, but other AMPK-independent pathways also contribute to the response... - Loss of cortical actin filaments in insulin-resistant skeletal muscle cells impairs GLUT4 vesicle trafficking and glucose transportAlicia M McCarthy
Dept of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA
Am J Physiol Cell Physiol 291:C860-8. 2006..We propose that a component of insulin-induced insulin resistance in skeletal muscle involves defects in PIP(2)/F-actin structure essential for insulin-regulated glucose transport... - Glucose transport and GLUT4 protein distribution in skeletal muscle of GLUT4 transgenic miceJ T Brozinick
Experimental Diabetes, Metabolism, and Nutrition Section, DB NIDDK National Institutes of Health, Bethesda, MD 20892 1420, USA
Biochem J 313:133-40. 1996..Furthermore, GLUT4 overexpression is not coupled to glucose-metabolic capacity... - Antidiabetogenic effects of chromium mitigate hyperinsulinemia-induced cellular insulin resistance via correction of plasma membrane cholesterol imbalanceEmily M Horvath
Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Center for Diabetes Research, Indianapolis, Indiana 46202, USA
Mol Endocrinol 22:937-50. 2008..These data predict a PM cholesterol basis for hyperinsulinemia-associated insulin resistance and importantly highlight the reversible nature of this abnormality... - 2-Alkoxydihydrocinnamates as PPAR agonists. Activity modulation by the incorporation of phenoxy substituentsJosé A Martín
Lilly Research Laboratories, Division of Eli Lilly and Company, Lilly S A, Alcobendas 28108, Madrid, Spain
Bioorg Med Chem Lett 15:51-5. 2005..Compound 1b (LY519818) was selected from our SAR studies to be advanced to clinical evaluation for the treatment of type II diabetes... - FGF-21 as a novel metabolic regulatorAlexei Kharitonenkov
Lilly Research Laboratories, Division of Eli Lilly and Co, Indianapolis, Indiana 46285, USA
J Clin Invest 115:1627-35. 2005..Thus, we conclude that FGF-21, which we have identified as a novel metabolic factor, exhibits the therapeutic characteristics necessary for an effective treatment of diabetes... - A tailored therapy for the metabolic syndrome: the dual peroxisome proliferator-activated receptor-alpha/gamma agonist LY465608 ameliorates insulin resistance and diabetic hyperglycemia while improving cardiovascular risk factors in preclinical modelsGarret J Etgen
Division of Endocrine Research, Lilly Research Laboratories, Eli Lilly, Indianapolis, Indiana 46285, USA
Diabetes 51:1083-7. 2002.... - Tetrahydroisoquinoline PPARgamma agonists: design of novel, highly selective non-TZD antihyperglycemic agentsJames R Henry
Lilly Research Laboratories, A Division of Eli Lilly and Company, Lilly Corporate Center, Indianapolis, IN 46285, USA
Bioorg Med Chem Lett 16:6293-7. 2006..Novel tetrahydroisoquinolines have been developed as potent PPAR ligands. Evaluation of these compounds in PPARgamma responsive models of type 2 diabetes is described... - Synthesis and evaluation of aminomethyl dihydrocinnamates as a new class of PPAR ligandsAlan M Warshawsky
Eli Lilly and Co, Indianapolis, IN 46285, USA
Bioorg Med Chem Lett 16:6328-33. 2006..Several compounds in this series have demonstrated potent plasma glucose and triglyceride lowering capability in rodent models of type 2 diabetes... - A peroxisome proliferator-activated receptor alpha/gamma dual agonist with a unique in vitro profile and potent glucose and lipid effects in rodent models of type 2 diabetes and dyslipidemiaAnne Reifel-Miller
Endocrinology Division, Lilly Research Laboratories, Indianapolis, Indiana 46285, USA
Mol Endocrinol 19:1593-605. 2005..These findings show that PPARgamma full agonist activity is not necessary to achieve potent and efficacious insulin-sensitizing benefits and demonstrate the therapeutic advantages of a PPARalpha/gamma dual agonist... - Measurement of contraction-stimulated GLUT-4 translocation in isolated skeletal muscleJoseph T Brozinick
Endocrine Division, Eli Lilly and Co, Indianapolis, IN, USA
Methods Mol Med 83:163-9. 2003 - Inhibition of ceramide synthesis ameliorates glucocorticoid-, saturated-fat-, and obesity-induced insulin resistanceWilliam L Holland
Division of Endocrinology, Metabolism, and Diabetes, Department of Internal Medicine, University of Utah, Salt Lake City, UT 84132, USA
Cell Metab 5:167-79. 2007..Second, they identify enzymes required for ceramide synthesis as therapeutic targets for combating insulin resistance caused by nutrient excess or glucocorticoid therapy...