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
43 Reads
  • 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
  • Source
    • "Although childhood obesity often persists into adulthood, the pathological processes of obesity-related morbidities begin in childhood (Biro & Wien, 2010). Obesity is strongly associated with a constellation of metabolic disorders marked by abdominal obesity, glucose intolerance, dyslipidemia, high blood pressure, and elevated proinflammatory markers (Després et al., 2008; Huang, Ball, & Franks, 2007). The early stages of atherosclerosis, the leading cause of cardiovascular and cerebrovascular events, can appear in utero, during infancy, or throughout childhood (Napoli et al., 1997, 1999). "
    [Show abstract] [Hide abstract]
    ABSTRACT: The prevalence of childhood obesity in the United States has tripled since the 1980s and is strongly linked to the early onset of several metabolic diseases. Recent studies indicate that lower cognitive function may be another complication of childhood obesity. This review considers the research to date on the role of obesity and nutrition on childhood cognition and brain health. Although a handful of studies point to a maladaptive relationship between obesity and aspects of cognitive control, remarkably little is known regarding the impact of fat mass on brain development and cognitive function. Further, missing from the literature is the role of nutrition in the obesity-cognition interaction. Nutrition may directly or indirectly influence cognitive performance via several pathways including provision of key substrates for optimal brain health, modulation of gut microbiota, and alterations in systemic energy balance. However, in the absence of malnutrition, the functional benefits of specific nutrient intake on particular cognitive domains are not well characterized. Here, we examine the literature linking childhood obesity and cognition while considering the effects of nutritional intake. Possible mechanisms for these relationships are discussed and suggestions are made for future study topics. Although childhood obesity prevalence rates in some developed countries have recently stabilized, significant disparities remain among groups based on sex and socioeconomic status. Given that the elevated prevalence of pediatric overweight and obesity may persist for the foreseeable future, it is crucial to develop a comprehensive understanding of the influence of obesity and nutrition on cognition and brain health in the pediatric population.
    Monographs of the Society for Research in Child Development 12/2014; 79(4):51-71. DOI:10.1111/mono.12130 · 5.50 Impact Factor
Show more