Genomes and Genes
Kyle L Hoehn
Affiliation: University of Virginia
- Insulin resistance is a cellular antioxidant defense mechanismKyle L Hoehn
Diabetes and Obesity Program, Garvan Institute of Medical Research, 384 Victoria Street, Darlinghurst, NSW 2010, Australia
Proc Natl Acad Sci U S A 106:17787-92. 2009..These data place mitochondrial superoxide at the nexus between intracellular metabolism and the control of insulin action potentially defining this as a metabolic sensor of energy excess...
- IRS1-independent defects define major nodes of insulin resistanceKyle L Hoehn
Diabetes and Obesity Program, Garvan Institute of Medical Research, Darlinghurst, NSW 2010, Australia
Cell Metab 7:421-33. 2008..These findings indicate that while insulin resistance is associated with multiple deficiencies, the most deleterious defects and the origin of insulin resistance occur independently of IRS...
- Global phosphoproteomics identifies a major role for AKT and 14-3-3 in regulating EDC3Mark Larance
Diabetes and Obesity Program, Garvan Institute of Medical Research, Sydney, Australia
Mol Cell Proteomics 9:682-94. 2010..These data highlight an important new arm of the insulin signaling cascade in the regulation of mRNA utilization...
- Acute or chronic upregulation of mitochondrial fatty acid oxidation has no net effect on whole-body energy expenditure or adiposityKyle L Hoehn
Garvan Institute of Medical Research, Darlinghurst, NSW, Australia
Cell Metab 11:70-6. 2010..We conclude that negative energy balance is a prerequisite for weight reduction, and increased fatty acid oxidation per se has little, if any, effect to reduce adiposity...
- CaMKII-mediated phosphorylation of the myosin motor Myo1c is required for insulin-stimulated GLUT4 translocation in adipocytesMing Fai Yip
Diabetes and Obesity Research Program, Garvan Institute of Medical Research, Darlinghurst, NSW 2010, Australia
Cell Metab 8:384-98. 2008..These data suggest that insulin regulates Myo1c function via CaMKII-dependent phosphorylation, and these events play a role in insulin-regulated GLUT4 trafficking in adipocytes likely involving Myo1c motor activity...
- Excess lipid availability increases mitochondrial fatty acid oxidative capacity in muscle: evidence against a role for reduced fatty acid oxidation in lipid-induced insulin resistance in rodentsNigel Turner
Diabetes and Obesity Program, Garvan Institute of Medical Research, Darlinghurst, NSW, Australia
Diabetes 56:2085-92. 2007..These findings suggest that high lipid availability does not lead to intramuscular lipid accumulation and insulin resistance in rodents by decreasing muscle mitochondrial fatty acid oxidative capacity...