Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PL008

Prize Lectures

Skeletal muscle mediators and exercise-induced adaptations governing insulin sensitivity in type 2 diabetes

J. Zierath1,2

1. Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden. 2. Center for Basic Metabolic Research, University of Copenhagen, Copenhagen, Denmark.

Type 2 diabetes mellitus is a life threatening metabolic disease reaching epidemic proportions. Although the molecular basis for this pathology is incompletely understood, genetic and environmental factors, probably in a synergistic manner, contribute to the risk of developing Type 2 diabetes. Type 2 diabetes shares many features of "accelerated aging" including insulin resistance, defective oxidative metabolism/mitochondrial function and loss of muscle mass. Strikingly, long-term participation in exercise training programs prevents insulin resistance and maintains functional muscle mass. The overarching goal of our research is to identify and validate molecules, pathways and ultimately new treatments that confer the benefits of exercise to improve glucose homeostasis and attenuate loss of strength and power throughout the lifespan. The circadian clock, an intrinsic molecular system in virtually all cells, is a key element in homeostatic regulation that controls a large array of metabolic genes. Thus, we are also addressing whether synchronizing exercise and nutrient interventions to the molecular circadian clock will maximize the health promoting benefits of exercise to enhance insulin sensitivity and prevent Type 2 diabetes. This lecture will present new evidence regarding exercise-responsive treatment targets and optimal intervention strategies to prevent metabolic disease.

Where applicable, experiments conform with Society ethical requirements