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1 Department of Medicine, University of Wisconsin, Madison, WI, USA
2 Department of Medicine, University of Wisconsin, Madison, WI, USA; Department of Physiology, University of Wisconsin, Madison, WI, USA
* To whom correspondence should be addressed. E-mail: kws{at}medicine.wisc.edu.
Activation of adenosine monophosphate activated protein kinase (AMPK) plays a
central role in allowing cells to adapt to nutrient deprivation in vitro. This link between
AMPK activity and nutritional status has raised the possibility that AMPK plays a role in
the metabolic adaptation to acute and chronic nutritional stress. However, the effects of
nutritional stress on AMPK activity in vivo have not been systematically evaluated. To
address this, we measured the effects of 24-hours of fasting and 4 months of caloric
restriction (CR) on AMPK 
1 and 2 activities in heart, skeletal muscle and liver in mice.
While fasting caused the expected changes in body weight, plasma leptin and free fatty
acids, it did not increase AMPK activity in heart or skeletal muscle, and only increased
liver AMPK activity by approximately 20% (p=0.10). Likewise, CR caused the expected
changes in body weight, plasma leptin and free fatty acids, but did not alter AMPK
activity in any of the three tissues. Although CR did not alter liver AMPK activity, it
dramatically decreased the amount of phosphorylated acetyl CoA carboxylase (ACC),
and this was found to be due to decreased protein expression. Plasma leptin, a putative
activator of AMPK, varied 8-fold across the four groups of mice in the absence of
changes in AMPK activity in any tissue. We conclude that while the metabolic
adaptations to fasting and CR include changes in plasma leptin concentration and P-ACC,
these effects occur without changes in AMPK activity.
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