1. Diabetes primes neutrophils to undergo NETosis, which impairs wound healing.

    Nature Medicine 21(7):815 (2015) PMID 26076037

    Wound healing is impaired in diabetes, resulting in significant morbidity and mortality. Neutrophils are the main leukocytes involved in the early phase of healing. As part of their anti-microbial defense, neutrophils form extracellular traps (NETs) by releasing decondensed chromatin lined with ...
  2. Severe insulin resistance alters metabolism in mesenchymal progenitor cells.

    Endocrinology 156(6):2039 (2015) PMID 25811318 PMCID PMC4430624

    Donohue syndrome (DS) is characterized by severe insulin resistance due to mutations in the insulin receptor (INSR) gene. To identify molecular defects contributing to metabolic dysregulation in DS in the undifferentiated state, we generated mesenchymal progenitor cells (MPCs) from induced pluri...
  3. Differential Role of Insulin/IGF-1 Receptor Signaling in Muscle Growth and Glucose Homeostasis.

    Cell Reports 11(8):1220 (2015) PMID 25981038 PMCID PMC4449334

    Insulin and insulin-like growth factor 1 (IGF-1) are major regulators of muscle protein and glucose homeostasis. To determine how these pathways interact, we generated mice with muscle-specific knockout of IGF-1 receptor (IGF1R) and insulin receptor (IR). These MIGIRKO mice showed >60% decrease ...
  4. Insulin resistance in brain alters dopamine turnover and causes behavioral disorders.

    PNAS 112(11):3463 (2015) PMID 25733901 PMCID PMC4371978

    Diabetes and insulin resistance are associated with altered brain imaging, depression, and increased rates of age-related cognitive impairment. Here we demonstrate that mice with a brain-specific knockout of the insulin receptor (NIRKO mice) exhibit brain mitochondrial dysfunction with reduced m...
  5. Differential effects of angiopoietin-like 4 in brain and muscle on regulation of lipoprotein lipase activity.

    Molecular Metabolism 4(2):144 (2015) PMID 25685701 PMCID PMC4314546

    Lipoprotein lipase (LPL) is a key regulator of circulating triglyceride rich lipoprotein hydrolysis. In brain LPL regulates appetite and energy expenditure. Angiopoietin-like 4 (Angptl4) is a secreted protein that inhibits LPL activity and, thereby, triglyceride metabolism, but the impact of Ang...
  6. Differential effects of angiopoietin-like 4 in brain and muscle on regulation of lipoprotein lipase activity.

    Molecular Metabolism 4(2):144 (2015) PMID 25685701

    Lipoprotein lipase (LPL) is a key regulator of circulating triglyceride rich lipoprotein hydrolysis. In brain LPL regulates appetite and energy expenditure. Angiopoietin-like 4 (Angptl4) is a secreted protein that inhibits LPL activity and, thereby, triglyceride metabolism, but the impact of Ang...
  7. Differential effects of angiopoietin-like 4 in brain and muscle on regulation of lipoprotein lipase activity.

    Molecular Metabolism 4(2):144 (2015) PMID 25685701 PMCID PMC4314546

    Lipoprotein lipase (LPL) is a key regulator of circulating triglyceride rich lipoprotein hydrolysis. In brain LPL regulates appetite and energy expenditure. Angiopoietin-like 4 (Angptl4) is a secreted protein that inhibits LPL activity and, thereby, triglyceride metabolism, but the impact of Ang...
  8. Differential effects of angiopoietin-like 4 in brain and muscle on regulation of lipoprotein lipase activity.

    Molecular Metabolism 4(2):144 (2015) PMID 25685701 PMCID PMC4314546

    Lipoprotein lipase (LPL) is a key regulator of circulating triglyceride rich lipoprotein hydrolysis. In brain LPL regulates appetite and energy expenditure. Angiopoietin-like 4 (Angptl4) is a secreted protein that inhibits LPL activity and, thereby, triglyceride metabolism, but the impact of Ang...
  9. Differential effects of angiopoietin-like 4 in brain and muscle on regulation of lipoprotein lipase activity.

    Molecular Metabolism 4(2):144 (2015) PMID 25685701 PMCID PMC4314546

    Lipoprotein lipase (LPL) is a key regulator of circulating triglyceride rich lipoprotein hydrolysis. In brain LPL regulates appetite and energy expenditure. Angiopoietin-like 4 (Angptl4) is a secreted protein that inhibits LPL activity and, thereby, triglyceride metabolism, but the impact of Ang...
  10. Differential effects of angiopoietin-like 4 in brain and muscle on regulation of lipoprotein lipase activity.

    Molecular Metabolism 4(2):144 (2015) PMID 25685701 PMCID PMC4314546

    Lipoprotein lipase (LPL) is a key regulator of circulating triglyceride rich lipoprotein hydrolysis. In brain LPL regulates appetite and energy expenditure. Angiopoietin-like 4 (Angptl4) is a secreted protein that inhibits LPL activity and, thereby, triglyceride metabolism, but the impact of Ang...
  11. Interplay between FGF21 and insulin action in the liver regulates metabolism.

    Journal of Clinical Investigation 125(1):458 (2015) PMID 25654556

  12. FoxO1 integrates direct and indirect effects of insulin on hepatic glucose production and glucose utilization.

    Nature Communications 6:7079 (2015) PMID 25963540

    FoxO proteins are major targets of insulin action. To better define the role of FoxO1 in mediating insulin effects in the liver, we generated liver-specific insulin receptor knockout (LIRKO) and IR/FoxO1 double knockout (LIRFKO) mice. Here we show that LIRKO mice are severely insulin resistant b...
  13. Erratum: FoxO1 integrates direct and indirect effects of insulin on hepatic glucose production and glucose utilization.

    Nature Communications 6:7861 (2015) PMID 26206703

  14. Interplay between FGF21 and insulin action in the liver regulates metabolism.

    Journal of Clinical Investigation 125(1):458 (2015) PMID 25654556

  15. Genetic Insulin Resistance Is a Potent Regulator of Gene Expression and Proliferation in Human iPS Cells.

    Diabetes 63(12):4130 (2014) PMID 25059784 PMCID PMC4238001

    Insulin resistance is central to diabetes and metabolic syndrome. To define the consequences of genetic insulin resistance distinct from those secondary to cellular differentiation or in vivo regulation, we generated induced pluripotent stem cells (iPSCs) from individuals with insulin receptor m...
  16. Genetic Insulin Resistance Is a Potent Regulator of Gene Expression and Proliferation in Human iPS Cells.

    Diabetes 63(12):4130 (2014) PMID 25059784 PMCID PMC4238001

    Insulin resistance is central to diabetes and metabolic syndrome. To define the consequences of genetic insulin resistance distinct from those secondary to cellular differentiation or in vivo regulation, we generated induced pluripotent stem cells (iPSCs) from individuals with insulin receptor m...
  17. Genetic insulin resistance is a potent regulator of gene expression and proliferation in human iPS cells.

    Diabetes 63(12):4130 (2014) PMID 25059784 PMCID PMC4238001

    Insulin resistance is central to diabetes and metabolic syndrome. To define the consequences of genetic insulin resistance distinct from those secondary to cellular differentiation or in vivo regulation, we generated induced pluripotent stem cells (iPSCs) from individuals with insulin receptor m...
  18. Genetic insulin resistance is a potent regulator of gene expression and proliferation in human iPS cells.

    Diabetes 63(12):4130 (2014) PMID 25059784 PMCID PMC4238001

    Insulin resistance is central to diabetes and metabolic syndrome. To define the consequences of genetic insulin resistance distinct from those secondary to cellular differentiation or in vivo regulation, we generated induced pluripotent stem cells (iPSCs) from individuals with insulin receptor m...
  19. Insulin and insulin-like growth factor 1 receptors are required for normal expression of imprinted genes.

    PNAS 111(40):14512 (2014) PMID 25246545 PMCID PMC4209990

    In addition to signaling through the classical tyrosine kinase pathway, recent studies indicate that insulin receptors (IRs) and insulin-like growth factor 1 (IGF1) receptors (IGF1Rs) can emit signals in the unoccupied state through some yet-to-be-defined noncanonical pathways. Here we show that...
  20. Insulin and insulin-like growth factor 1 receptors are required for normal expression of imprinted genes.

    PNAS 111(40):14512 (2014) PMID 25246545 PMCID PMC4209990

    In addition to signaling through the classical tyrosine kinase pathway, recent studies indicate that insulin receptors (IRs) and insulin-like growth factor 1 (IGF1) receptors (IGF1Rs) can emit signals in the unoccupied state through some yet-to-be-defined noncanonical pathways. Here we show that...