Abstract

Patients with the metabolic syndrome are characterized by insulin resistance, obesity and a predisposition to hypertension, dyslipidaemia, pancreatic -cell dysfunction, type 2 diabetes and premature atherosclerosis. Here we review the hypothesis that a common feature linking these multiple abnormalities is dysregulation of the AMP-activated protein kinase (AMPK)/malonyl-CoA fuel-sensing and signalling network. It is proposed that such dysregulation leads to alterations in cellular fatty-acid metabolism that in turn cause ectopic lipid accumulation, cellular dysfunction and ultimately disease. Evidence is also presented that factors that activate AMP kinase and/or reduce malonyl-CoA levels might reverse these abnormalities or prevent them from occurring.

Author affiliations

1. Departments of Medicine and Physiology and Biophysics, Boston University School of Medicine and Diabetes Unit, Section of Endocrinology, Boston Medical Center, 715 Albany Street, Boston, Massachusetts 02118, USA.
   Email: nruderman@medicine.bu.edu
2. Molecular Nutrition Unit, Departments of Nutrition and Biochemistry, University of Montreal, CR-CHUM, Pavillon de Séve Y4603, 1560 Sherbrooke East, Montreal, Quebec 214M1, Canada.
   Email: marc.prentki@umontreal.ca

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