Published online before print March 20, 2008, doi: 10.1161/ATVBAHA.107.159228
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© 2008 American Heart Association, Inc.
Brief Reviews |
Abdominal Obesity and the Metabolic Syndrome: Contribution to Global Cardiometabolic Risk
From the Hôpital Laval Research Centre (J.-P.D., I.L., P. Pibarot, P.M., E.L., J.R.-C., O.F.B., P. Poirier); the Institut universitaire de cardiologie et de pneumologie (J.-P.D., P.M., E.L., J.R.-C., O.F.B., P. Poirier), Hôpital Laval; the Division of Kinesiology (J.-P.D.), Department of Social and Preventive Medicine, Université Laval; the Lipid Research Centre (J.B.), CHUQ Research Centre; the Department of Medicine (P. Pibarot), Université Laval; the Department of Surgery (P.M.), Université Laval; the Faculty of Pharmacy (P. Poirier), Université Laval, Québec City, QC, Canada.
Correspondence to Jean-Pierre Després, PhD, FAHA, Scientific Director, International Chair on Cardiometabolic Risk, Director of Research, Cardiology, Hôpital Laval Research Centre, 2725 chemin Ste-Foy, Pavilion Marguerite-D’Youville, 4th Floor, Québec City, QC, G1V 4G5, CANADA. E-mail jean-pierre.despres{at}crhl.ulaval.ca
Series Editor: Marja-Riitta Taskinen
Metabolic Syndrome and Atherosclerosis
ATVB In Focus
Preview Brief Reviews in this Series:
•Grundy, SM. Metabolic syndrome pandemic. Arteroscler Thromb Vasc Biol. 2008;28:629–636.
•Barter PJ, Rye KA. Is there a role for fibrates in the management of dyslipidemia in the metabolic syndrome. Arteroscler Thromb Vasc Biol. 2008;28:39–46.
•Kotronen A, Yki-Järvinen. Fatty liver: a novel component of the metabolic syndrome. Arteroscler Thromb Vasc Biol. 2008;28:27–38.
•Gustafson B, Hammarstedt A, Andersson CX, and Smith U. Inflamed adipose tissue: a culprit underlying the metabolic syndrome and atherosclerosis. Arteroscler Thromb Vasc Biol. 2007;27:2276–2283.
There is currently substantial confusion between the conceptual definition of the metabolic syndrome and the clinical screening parameters and cut-off values proposed by various organizations (NCEP-ATP III, IDF, WHO, etc) to identify individuals with the metabolic syndrome. Although it is clear that in vivo insulin resistance is a key abnormality associated with an atherogenic, prothrombotic, and inflammatory profile which has been named by some the "metabolic syndrome" or by others "syndrome X" or "insulin resistance syndrome", it is more and more recognized that the most prevalent form of this constellation of metabolic abnormalities linked to insulin resistance is found in patients with abdominal obesity, especially with an excess of intra-abdominal or visceral adipose tissue. We have previously proposed that visceral obesity may represent a clinical intermediate phenotype reflecting the relative inability of subcutaneous adipose tissue to act as a protective metabolic sink for the clearance and storage of the extra energy derived from dietary triglycerides, leading to ectopic fat deposition in visceral adipose depots, skeletal muscle, liver, heart, etc. Thus, visceral obesity may partly be a marker of a dysmetabolic state and partly a cause of the metabolic syndrome. Although waist circumference is a better marker of abdominal fat accumulation than the body mass index, an elevated waistline alone is not sufficient to diagnose visceral obesity and we have proposed that an elevated fasting triglyceride concentration could represent, when waist circumference is increased, a simple clinical marker of excess visceral/ectopic fat. Finally, a clinical diagnosis of visceral obesity, insulin resistance, or of the metabolic syndrome is not sufficient to assess global risk of cardiovascular disease. To achieve this goal, physicians should first pay attention to the classical risk factors while also considering the additional risk resulting from the presence of abdominal obesity and the metabolic syndrome, such global risk being defined as cardiometabolic risk.
Key Words: global cardiometabolic risk • insulin resistance • metabolic syndrome • visceral obesity • waist circumference
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