Description.  Obesity related insulin resistance is a primary contributor to this increase in metabolic disease and is proposed to arise secondary to an inflammatory response caused by infiltration of adipose tissue (AT) with macrophages and pro-inflammatory cytokine production. Cellular signals within AT that cause the inflammatory phenotype are largely unknown. Phosphoinosital 3-kinase (PI3K) regulates key insulin, cytokine, and growth signaling pathways, and is thus a strong candidate for linking cellular insulin resistance with the inflammatory response. We are working on identifying novel signaling pathways linking PI3K to the inflammatory signaling cascade and characterization of alternative regulatory subunit isoforms, p55alpha and p50alpha. This work is funded by NIH R01DK095926.


Tools & Skills.    We use primarily transgenic mouse models to study the in vivo effect of altering the abundance (knockdown or over-expression) of signaling proteins on physiology & metabolism in the whole animal and isolated cells.

  • Mouse Phenotyping
    • Body composition by MRI
    • Metabolic and behavioral phenotyping in metabolic cages
    • Insulin sensitivity & glucose tolerance
    • Primary adipocyte cell isolation
    • Animal handling, surgery, dissection & husbandry
  • Cellular signaling & metabolism
    • Signaling pathways by immunoblotting, immunoprecipitation, ChIP
    • Gene expression by qPCR
    • Immunophenotyping by flow cytometry
    • Analysis of glucose uptake in isolated cells
  • Cell culture techniques & experiments
    • Gene manipulation by siRNA/over-expression
    • Fluorescence microscopy