August Krogh Seminar


Extramyocellular Adaptations in the Pathogenesis of Muscle Insulin Resistance

v/ David H. Wasserman, Director, Mouse Metabolic Phenotyping Center, Professor of Molecular Physiology and Biophysics, Vanderbilt-NIH Mouse Metabolic Phenotyping Center, Tennessee, USA.

Abstract

The regulation of muscle glucose uptake has traditionally been defined by the rate-limiting step paradigm, where membrane glucose transport is the sole determinant of control. 

Research from our laboratory in murine models, as well as the contributions of other laboratories have shown that muscle glucose uptake is more accurately defined by distributed control. Glucose flux into muscle is controlled by delivery of glucose to muscle, muscle membrane glucose transport, and phosphorylation of glucose within muscle. 

The implication of distributed control is that muscle insulin resistance may occur due to dysfunction at multiple sites. Recent work from our laboratory has combined pharmacological tools with genetic mouse models to demonstrate that insulin resistance due to high fat feeding is largely a consequence of remodeling of the muscle extracellular matrix and the abundance of capillaries.

Further we show that targeting extracellular matrix components, collagen receptor signaling, or muscle blood flow and capillary abundance improves insulin action in the diet-induced insulin resistant mouse.  Defects in the extracellular matrix may represent a common pathogenic link between the vascular, fibrotic, and metabolic co-aggregates of obesity.

Time

31 May 2013 14:00-15:30

Venue

Auditorium 1, August Krogh Building, Universitetsparken 13, DK-2100 Copenhagen

Registration

Participation is free, but please register here.

For PhD students

PhD students participating in August Krogh seminars receive 0,2 ECTS per seminar

Contact

Christian Frøsig, CFrosig@ifi.ku.dk, mobile +45 2875 1617 

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