Section for Integrative Physiology – University of Copenhagen

Role of AMP-activated protein kinase for regulating post-exercise insulin sensitivity

Research output: Chapter in Book/Report/Conference proceedingBook chapter

Skeletal muscle insulin resistance precedes development of type 2 diabetes (T2D). As skeletal muscle is a major sink for glucose disposal, understanding the molecular mechanisms involved in maintaining insulin sensitivity of this tissue could potentially benefit millions of people that are diagnosed with insulin resistance. Regular physical activity in both healthy and insulin-resistant individuals is recognized as the single most effective intervention to increase whole-body insulin sensitivity and thereby positively affect glucose homeostasis. A single bout of exercise has long been known to increase glucose disposal in skeletal muscle in response to physiological insulin concentrations. While this effect is identified to be restricted to the previously exercised muscle, the molecular basis for an apparent convergence between exercise- and insulin-induced signaling pathways is incompletely known. In recent years, we and others have identified the Rab GTPase-activating protein, TBC1 domain family member 4 (TBC1D4) as a target of key protein kinases in the insulin- and exercise-activated signaling pathways. Our working hypothesis is that the AMP-activated protein kinase (AMPK) is important for the ability of exercise to insulin sensitize skeletal muscle through TBC1D4. Here, we aim to provide an overview of the current available evidence linking AMPK to post-exercise insulin sensitivity.

Original languageEnglish
Title of host publicationAMP-activated Protein Kinase
EditorsM D Cordero, B Viollet
Number of pages46
Publication date2016
ISBN (Print)978-3-319-43587-9
ISBN (Electronic)978-3-319-43589-3
StatePublished - 2016
SeriesE X S

    Research areas

  • The Faculty of Science - AMP-activated protein kinase, Exercise, Skeletal muscle, Glucose uptake, TBC1D4, AS160, Insulin sensitivity

ID: 168911648