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Received April 12, 2006
Revised May 5, 2006
Accepted after revision May 12, 2006
1 INSERM U671; Universit éPierre et Marie Curie-Paris6
2 INSERM U671; Université Pierre et Marie Curie-Paris6
* To whom correspondence should be addressed. E-mail: pferre{at}bhdc.jussieu.fr.
AMP-activated protein kinase (AMPK) is involved in cellular energy homeostasis. In muscles and liver its functions have been extensively studied. AMPK stimulates pathways allowing to increase energy production (glucose transport, fatty acid oxidation) and switches off pathways which consume energy (lipogenesis, protein synthesis, gluconeogenesis). This has led to the concept that AMPK has an interesting pharmaceutical potential in situations of insulin resistance and it is indeed the target of existing drugs and hormones which improve insulin sensitivity. Adipose tissue is a key player in energy metabolism through the release of substrates and hormones involve in metabolism and insulin sensitivity. Activation of AMPK in adipose tissue can be achieved through situations such as fasting and exercise. Leptin and adiponectin as well as hypoglycaemic drugs are activators of adipose tissue AMPK. This activation probably involves changes in the AMP/ATP ratio and the upstream kinase LKB1. When activated, AMPK limits fatty acid efflux from adipocytes and favors local fatty acid oxidation. Since fatty acids have a key role in insulin resistance, specially in muscles, activating AMPK in adipose tissue might reveal beneficial in insulin resistant states all the more as AMPK activation also reduces cytokine secretion in adipocytes.
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