Jesper Bratz Birk

Jesper Bratz Birk

Academic staff

ResearcherID: D-3523-2015

Scopus ID: 7007150599

Primary fields of research

  • Intracellular insulin signaling and glucose metabolism
  • Characterization of 5’ AMP Activated Protein Kinase (AMPK)

Current research

  • My primary research areas are insulin and contraction stimulated glucose metabolism in skeletal muscle.  This involves analyses of proteins in the insulin signaling pathway ranging from the Insulin Receptor to GLUT4 exocytosis and glucose uptake to activation of Glycogen Synthase, which is responsible for the incorporation of glucose-6-phosphate into glycogen. In this regard we analyze skeletal muscle from mouse, rat and especially healthy humans compared to patients with Type 2 Diabetes, to elucidate the defects responsible for the insulin resistance in the diabetic patients.
  • The second mean focus area is the characterization of 5’ AMP Activated Protein Kinase (AMPK), being the primary fuel gauge in the cell, reaction to low energy levels in the cell leading the depression of anabolic processes and increased ATP production. AMPK is a heterotrimeric complex, which due to the existence of several subunit isoforms can be found in twelve different constitutions. The constitution of these complexes is being characterized in mouse, rat and human tissues, such as skeletal and heart muscle, liver and adipose tissue. When determined the activation of these complexes are analyzed in response to different stimuli, such as muscle contraction, hypoxia and chemical activation with more or less specific AMPK activators. Downstream targets of AMPK are also analyzed in response to AMPK activation, for example phosphorylation of Acetyl CoA Carboxylase and AS160, leading to increased lipid oxidation and glucose uptake, respectively.

Selected publications

  1. Published

    Predominant alpha2/beta2/gamma3 AMPK activation during exercise in human skeletal muscle

    Birk, Jesper Bratz & Wojtaszewski, Jørgen F P, 2006, In: Journal of Physiology. 577, 3, p. 1021-1032 12 p.

    Research output: Contribution to journalJournal articlepeer-review

ID: 1841140