Abdominal Obesity and the Metabolic Syndrome: Contribution to Global Cardiometabolic Risk

Hôpital Laval Research Centre, 2725 Chemin Ste-Foy, Pavilion Marguerite-D'Youville, 4th Floor, Québec City, QC G1V4G5, Canada.
Arteriosclerosis Thrombosis and Vascular Biology (Impact Factor: 6). 07/2008; 28(6):1039-49. DOI: 10.1161/ATVBAHA.107.159228
Source: PubMed


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.

Download full-text


Available from: Isabelle Lemieux, Jul 09, 2014
47 Reads
  • Source
    • "Additionally, the visceral fat is an important source of adipokines (interleukin-6, tumor necrosis factor-a, and adiponectin), all related to IR [30]. The hyperlipolytic state of VAT exposes the liver through the portal circulation to high concentrations of FFA, damaging several hepatic metabolic processes and leading to decreased insulin clearance (hyperinsulinemia), increased hepatic glucose production (glucose intolerance), and increased secretion of VLDL and apolipoprotein B (hypertriglyceridemia) [31]. Additionally , high serum concentrations of FFA overload the muscles and the liver with lipids that lead to IR [32]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: The aim of this study was to identify metabolically healthy obese individuals (MHOs) and their characteristics, as well as to estimate cardiovascular risk using the Framingham score. In all, 258 adult individuals, with body mass index ≥30 kg/m(2), and no report of diabetes mellitus or cardiovascular disease, were classified according to their metabolic state considering two criteria: rhe National Cholesterol Education Program-Adult Treatment Panel III (NCEP-ATP III) and the homeostasis model assessment (HOMA). Biochemical, anthropometric, and body composition characteristics were compared between MHOs and metabolically unhealthy obese (MUO) individuals according to each criterion. Cardiovascular risk was estimated using the Framingham score. MHOs exhibited smaller waist circumference and lower body fat percentage, as well as lower blood glucose, triacylglycerols, and insulin levels, in addition to higher high-density lipoprotein cholesterol concentration, when HOMA criterion (P < 0.05) and associated criteria were adopted. The estimated cardiovascular risk was similar between the two groups according to the HOMA index; however, the risk was significantly lower according to the ATP III guidelines. Obese individuals at intermediate and high risk showed higher body fat percentage compared with those individuals at low risk. MHOs had biochemical and anthropometric characteristics, such as lower body mass index, waist circumference, percent fat mass, glucose, triacylglycerols, and increased high-density lipoprotein, that made them different from those individuals classified as MUO. The latter exhibited increased risk for cardiovascular disease according to the Framingham score, when using the ATP III criterion alone or in conjunction with the HOMA index. Copyright © 2015 Elsevier Inc. All rights reserved.
    Nutrition 01/2015; 31(6). DOI:10.1016/j.nut.2014.12.024 · 2.93 Impact Factor
  • Source
    • "The cut off value of waist circumference is high than the standard cut off value for Asian Indian. The commonly used definitions to predict metabolic syndrome requires certain modification as waist circumference represent visceral fat, and several studies have shown the relationship to an increase risk of cardiovascular disease (Després et al., 2008; Chiba et al., 2007; Sam et al., 2009). Asian Indian have higher abdominal fat mass as compared to Caucasian and African American, the central obesity is been postulated as a leading modifiable cause of cardiovascular disease in Asia (Mohan & Deepa, 2006) The optimal cut off value for systolic and diastolic blood pressure is in accordance with cut off defined by standard criteria. "
    01/2015; 12(1):582. DOI:10.14687/ijhs.v12i1.3189
  • Source
    • "Altered glucose tolerance is one of the severe outcomes of excess fat mass [3] [4] [5]. The excessive development of visceral white adipose tissue (AT) is an important determinant of metabolic syndrome, a complication that frequently occurs in obese subjects [6]. Among the intra-abdominal depots, epididymal (EPI) and retroperitoneal (RET) AT are considered as visceral depots and have been largely used for metabolic regulation studies [7] [8] [9] [10] [11]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Scope: High-fat diet (HFD) increases visceral adipose tissue (AT). Our aim was to evaluate whether citrulline (CIT) affected nonesterified fatty acid (NEFA) metabolism in AT from HFD-fed rats. Methods and results: Rats were fed for 8 weeks with either a control diet (CD) or HFD. Retroperitoneal AT explants were exposed to 2.5 mmol/L CIT for 24 h. We analyzed lipolysis, beta-oxidation, glyceroneogenesis, and the expression of the key associated enzymes. CIT doubled NEFA release selectively in HFD AT. Phosphorylation of hormone-sensitive lipase was upregulated 50 and 100% by CIT in CD and HFD AT, respectively. Under CIT, beta-oxidation increased similarly whatever the diet, whereas glyceroneogenesis, which permits NEFA re-esterification, was downregulated 50 and 80% in CD and HFD AT, respectively. In the latter, the important decrease in re-esterification probably explains the rise of NEFA release. A pretreatment with the nitric oxide synthase inhibitor N ω-nitro-l-arginine methyl ester abolished CIT effects. Conclusion: These results demonstrate direct lipolytic and antiglyceroneogenic effects of CIT on CD and HFD AT. The selective CIT-mediated NEFA release from HFD AT was probably the consequence of the drastic decrease in glyceroneogenesis and nitric oxide was a mediator of CIT effects. These results provide evidence for a direct action of CIT on AT to reduce overweight.
    Molecular Nutrition & Food Research 12/2014; 58(12). DOI:10.1002/mnfr.201400507 · 4.60 Impact Factor
Show more