Andreas Mæchel Fritzen - Defining the role of AMPK in ApoA-1 induced glucose uptake and metabolism in skeletal muscle

Type 2 diabetes and the constituents of the metabolic syndrome are associated with low and dysfunctional high-density lipoprotein (HDL). The main protein component of HDL, apolipoprotein A-I (apoA-I), was recently assigned to a glucose controlling function, since administration of apoA-I to  cell cultures and in an insulin-resistant mouse model revealed an increase in glucose uptake and glucose tolerance, respectively.

In cell cultures, it was recently shown that AMP-activated protein kinase (AMPK) was activated by apoA-I and at the same time elevated glucose uptake. These findings suggest that the apoA-I-stimulated glucose uptake was dependent on AMPK. Whether this dependency of AMPK for apoA-I stimulated glucose uptake is maintained in intact skeletal muscle remains to be elucidated. Thus, by proof-of-concept studies using genetic ablation of AMPK activity in skeletal muscle of mice, in this 1-year post doc project I want to explore the role of AMPK in the apoA-I effects on glucose uptake in skeletal muscle.