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The role of leg and splanchnic tissues in the metabolism of triglyceride fatty acid (TGFA) and gender-related differences in fatty acid metabolism were analyzed in nonobese men and women. Male subjects exhibiting greater visceral fat and lesser leg fat compared to female subjects exhibited greater basal plasma insulin concentrations. Furthermore, both male and female subjects exhibited also similar plasma glucose levels. However, male subjects have higher rates of meal fatty acid disposal in their splanchnic tissues.

Hyperhomocysteinemia (HH) and metabolic syndrome (MS) are associated with increased cardiovascular risk. However, whether there is a link between MS or its components and homocysteine levels in a population without cardiovascular disease is not well established. We conducted a case-control study in 61 MS patients (41 males, 20 females, aged 51 ± 11 years) and in 98 controls without MS (59 males, 39 females, aged 50 ± 10 years) to ascertain the association between MS and HH, and with inflammatory markers. MS was classified according to the updated ATPIII criteria [17]. No differences in homocysteine levels were observed when comparing MS patients and controls (12.0 ± 3.18 μM vs. 11.9 ± 3.5 μM, p = 0.829). No association was found between HH (homocysteine >15 μM) and MS, its components (abdominal obesity (p = 0.635), hypertension (0.229), low-HDL cholesterol (p = 0.491), glucose >100 mg/dL (0.485), hypertriglyceridemia (p = 0.490)) or the number of MS components (p = 272). When considering glucose >110 mg/dL (NCEP-ATPIII criteria, 2001) instead of glucose intolerancen >100 mg/dl (updated ATPIII criteria, Grundy, 2005), a borderline association with HH was observed (p = 0.054) of statistical significance (p = 0.008) when glucose >126 mg/dL was considered. In a multivariate regression model, creatinine, folic acid and vitamin B12 were the only independent predictors of homocysteine levels (p < 0.05). Although MS correlated with inflammatory parameters (fibrinogen, hs-RCP, plasma viscosity and leukocyte count, p < 0.001), no association was found between HH and the above-mentioned parameters (p > 0.05). Our results do not indicate a link between SM or its individual components with HH, and diabetes was the only relevant contribution. Cardiovascular disease risk due to MS and HH seems to share no common mechanisms. [ABSTRACT FROM AUTHOR]

In order to characterize the metabolic syndrome it becomes necessary to establish a number of diagnostic criteria. Because of its impact on cardiovascular morbidity/mortality, considerable attention has been focussed on the dyslipidemia accompanying the metabolic syndrome.The aim of this review is to highlight the fundamental aspects of the pathophysiology, diagnosis, and the treatment of the metabolic syndrome dyslipidemia with recommendations to clinicians.The clinical expression of the metabolic syndrome dyslipidemia is characterized by hypertriglyceridemia and low levels of high-density lipoprotein-cholesterol (HDL-C). In addition, metabolic syndrome dyslipidemia is associated with high levels of apolipoprotein (apo) B-100-rich particles of a particularly atherogenic phenotype (small dense low-density lipoprotein-cholesterol [LDL-C]. High levels of triglyceride-rich particles (very low-density lipoprotein) are also evident both at baseline and in overload situations (postprandial hyperlipidemia). Overall, the ‘quantitative’ dyslipidemia characterized by hypertriglyceridemia and low levels of HDL-C and the ‘qualitative’ dyslipidemia characterized by high levels of apo B-100- and triglyceride-rich particles, together with insulin resistance, constitute an atherogenic triad in patients with the metabolic syndrome.The therapeutic management of the metabolic syndrome, regardless of the control of the bodyweight, BP, hyperglycemia or overt diabetes mellitus, aims at maintaining optimum plasma lipid levels. Therapeutic goals are similar to those for high-risk situations because of the coexistence of multiple risk factors. The primary goal in treatment should be achieving an LDL-C level of <100 mg/dL (or <70 mg/dL in cases with established ischemic heart disease or risk equivalents). A further goal is increasing the HDL-C level to ≥40 mg/dL in men or 50 mg/dL in women. A non-HDL-C goal of 130 mg/dL should also be aimed at in cases of hypertriglyceridemia.Lifestyle interventions, such as maintaining an adequate diet, and a physical activity program, constitute an essential part of management. Nevertheless, when pharmacologic therapy becomes necessary, fibrates and HMG-CoA reductase inhibitors (statins) are the most effective drugs in controlling the metabolic syndrome hyperlipidemia, and are thus the drugs of first choice. Fibrates are effective in lowering triglycerides and increasing HDL-C levels, the two most frequent abnormalities associated with the metabolic syndrome, and statins are effective in lowering LDL-C levels, even though hypercholesterolemia occurs less frequently. In addition, the combination of fibrates and statins is highly effective in controlling abnormalities of the lipid profile in patients with the metabolic syndrome. [ABSTRACT FROM AUTHOR]