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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.

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Background-The present study tested the hypothesis that simple variables, such as waist circumference and fasting plasma triglyceride (TG) concentrations, could be used as screening tools for the identification of men characterized by a metabolic triad of nontraditional risk factors (elevated insulin and apolipoprotein [apo] B and small, dense LDL particles). Methods and Results-Results of the metabolic study (study 1) conducted on 185 healthy men indicate that a large proportion (Ͼ80%) of men with waist circumference values Ն90 cm and with elevated TG levels (Ն2.0 mmol/L) were characterized by the atherogenic metabolic triad. Validation of the model in an angiographic study (study 2) on a sample of 287 men with and without coronary artery disease (CAD) revealed that only men with both elevated waist and TG levels were at increased risk of CAD (odds ratio of 3.6, PϽ0.03) compared with men with low waist and TG levels. Conclusions-It is suggested that the simultaneous measurement and interpretation of waist circumference and fasting TG could be used as inexpensive screening tools to identify men characterized by the atherogenic metabolic triad (hyperinsulinemia, elevated apo B, small, dense LDL) and at high risk for CAD. (Circulation. 2000;102:179-184.)

Variation in the TC/HDL-C ratio may be associated with more substantial alterations in metabolic indices predictive of ischemic heart disease risk and related to the insulin resistance syndrome than variation in the LDL-C/HDL-C ratio.

Alirocumab produced greater LDL-C reductions than ezetimibe in statin-intolerant patients, with fewer skeletal-muscle adverse events vs atorvastatin.

Although metabolic disturbances are often observed in obese patients, increased accumulation of visceral adipose tissue (AT) has been shown to be more closely associated with high fasting triglyceride (TG) and insulin levels as well as with low HDL cholesterol concentrations than with excess body fatness per se. Interestingly, the fasting concentration of plasma TGs has been shown to be an important determinant of the magnitude and duration of the postprandial TG response. Yet little is known about the respective contributions of obesity versus excess visceral AT to the variation in postprandial TG clearance. In the present study, we examined potential differences in postprandial triglyceride-rich lipoprotein (TRL) responses in subjects characterized by high versus low levels of visceral AT. In a sample of 43 men (mean age: 41.3 +/- 9.6 years), we found that both excess body fat and visceral obesity were associated with increased postprandial TG responses in total TRL (r = 0.33-0.45). We also found a strong relationship between fasting plasma TG levels and postprandial total TRL-TG concentrations (r = 0.79, P < 0.0001). When matched for total body fat mass, individuals with high levels of visceral AT (> or =130 cm2; n = 10) as assessed by computed tomography were characterized by increased medium- and small-TRL-TG responses (P < 0.05) compared with subjects with low visceral AT accumulation (<130 cm2; n = 10). Moreover, this elevated response of small-TRL triglycerides noted in men with high levels of visceral AT was not accompanied by a concomitant increased retinyl palmitate response in this TRL fraction, suggesting that visceral obesity in men is accompanied by higher postprandial VLDL production than is found in obese men with lower levels of visceral AT. Increased postprandial insulin and free fatty acid (FFA) responses were also noted in men with high levels of visceral AT. Finally, postheparin plasma lipoprotein lipase activity was negatively correlated with the total-TRL-TG response in a subsample of 32 individuals (r = -0.37, P < 0.05). The results of the present study suggest that visceral obesity is associated with an impaired postprandial TG clearance. Furthermore, the exaggerated postprandial FFA response observed in subjects with high visceral AT suggests that visceral obesity may contribute to fasting and postprandial hypertriglyceridemia by altering FFA metabolism in the postprandial state.

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