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Metabolic Syndrome: Adenosine Monophosphate‐activated Protein Kinase and Malonyl Coenzyme A
Author(s) -
Ruderman Neil B.,
Saha Asish K.
Publication year - 2006
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1038/oby.2006.279
Subject(s) - adenosine monophosphate , adenosine , protein kinase a , chemistry , coenzyme a , endocrinology , medicine , biochemistry , kinase , enzyme , reductase
The metabolic syndrome can be defined as a state of metabolic dysregulation characterized by insulin resistance, central obesity, and a predisposition to type 2 diabetes, dyslipidemia, premature atherosclerosis, and other diseases. An increasing body of evidence has linked the metabolic syndrome to abnormalities in lipid metabolism that ultimately lead to cellular dysfunction. We review here the hypothesis that, in many instances, the cause of these lipid abnormalities could be a dysregulation of the adenosine monophosphate‐activated protein kinase (AMPK)/malonyl coenzyme A (CoA) fuel‐sensing and signaling mechanism. Such dysregulation could be reflected by isolated increases in malonyl CoA or by concurrent changes in malonyl CoA and AMPK, both of which would alter intracellular fatty acid partitioning. The possibility is also raised that pharmacological agents and other factors that activate AMPK and/or decrease malonyl CoA could be therapeutic targets.