Objective: Studies on the prevalence of metabolic syndrome (MS) in European obese children using child-based criteria are scanty. Moreover, it is unknown if nontraditional cardiovascular disease (CVD) risk factors are associated with the MS at this early age in these subjects. Design and subjects: We studied the prevalence of the MS in 588 Caucasian obese children and adolescents by devising a World Health Organization derived definition and child-specific criteria, whose deviation from normalcy was based on an age, sex, and ethnically comparable control group of 1363 subjects. In a subgroup of 206 obese children, we investigated the association of the MS with nontraditional CVD risk factors. Measurements: Fasting blood samples for glucose and lipids measurements were taken in both control and obese children. In addition, the obese children underwent an oral glucose tolerance test. In the subgroup of 206 obese children, albumin excretion rate , plasma uric acid, fibrinogen, plasminogen activator inhibitor type 1(PAI-1), C-reactive protein, interleukin 6 and white blood cells were also measured. Results: The prevalence of MS was 23.3%. A similar prevalence of 23% of MS was recorded in the subgroup of 206 obese children in whom measurements of nontraditional CVD risk factors were available. After adjustment for the degree of obesity, subjects with MS had significantly higher uric acid (6.670.23 vs 6.170.12 mg/dl, Po0.0001) and PAI-1 plasma concentrations (231.4725.50 vs 214.3712.96 ng/ml, Po0.05) and a higher frequency of microalbuminuria (37 vs 20%, Po0.05) than those without MS. Microalbuminuria, uric acid and PAI-1 explained 10.6% of the variance of MS. Conclusion: Approximately, a quarter of Caucasian obese children have the MS. The association of MS with several nontraditional risk factors for CVD early in life suggests a heightened CVD risk in these individuals.

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Objective: The role of glucocorticoids production in adipose tissue in the development of metabolic disorders in humans has not been fully characterized. We investigated whether in obese subjects, 11b-hydroxysteroid dehydrogenase type 1 (11b-HSD1) expression in subcutaneous (SAT) and visceral (VAT) adipose tissue is associated with the occurrence of metabolic disorders and the expression of adiponectin and tumor necrosis factor a (TNFa) and two glucocorticoid-regulated adipokines able to influence the metabolic control. Design and subjects: Sixty-two obese patients were enrolled in the study. SAT and VAT samples were obtained from 13 patients undergoing bariatric surgery (body mass index (BMI) 39.175.3 kg/m 2 ). SAT samples were obtained from 49 patients who underwent periumbilical biopsy (BMI 36.975.1 kg/m 2 ). Measurements: Oral glucose tolerance tests in subjects without known diabetes. Circulating glucose, lipid, insulin, adiponectin, TNFa and urinary-free cortisol levels. Real-time PCR to quantify mRNA levels of 11b-HSD1, hexose-6-phosphate dehydrogenase (H6PDH), adiponectin and TNFa. Western blot analysis to evaluate 11b-HSD1 protein expression. Results: In the majority of the obese subjects, VAT expresses more 11b-HSD1 than SAT. VAT 11b-HSD1 expression was not associated with metabolic disorders. SAT 11b-HSD1 mRNA levels were higher in subjects with than in those without metabolic syndrome (Po0.05) and in patients with type 2 diabetes compared to patients with impaired or normal glucose tolerance (Po0.0001). SAT 11b-HSD1 expression was independently related to fasting glucose (Po0.0001) and urinary-free cortisol levels (Po0.01), and increased expression of 11b-HSD1 was associated with increased adiponectin and TNFa expression and decreased serum adiponectin levels (all P's o0.05). Conclusions: In obese subjects, increased 11b-HSD1 expression in SAT, but not in VAT, is associated with the worsening of metabolic conditions. We hypothesize that higher glucocorticoid production in adipose tissue would favor the development of metabolic disorders through a decrease in adiponectin release.

Objective: The effects of metformin on adiponectin production are controversial and have never been investigated in human adipose tissue. We analysed whether metformin modulates, in vitro and in vivo, gene expression, protein content, and secretion of adiponectin. Methods: For the in vitro study, subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) samples from 5 non-diabetic obese patients were collected. For the in vivo investigation, 22 obese patients were randomly assigned to metformin+lifestyle (ML) or placebo+lifestyle (PL) intervention. SAT specimens and blood samples were collected before and after the intervention in both groups. Results: In in vitro experiments, treatment with metformin increased the expression and secretion of adiponectin in SAT, but not in VAT explants. In the in vivo study, a significant increase in adiponectin and a decreased expression of a macrophage activation marker (CD68) were observed only in SAT of the ML group. Conclusion: These results demonstrate that metformin is able to up-regulate adiponectin gene expression, both in vivo and in vitro, and to stimulate adiponectin protein secretion from human SAT in vitro. It could be hypothesised that metformin-induced adiponectin increase within adipose tissue may have an unexpected role in the reduction of local inflammation.

BACKGROUND: Left ventricular hypertrophy (LVH) and prolonged QT interval at ECG (QTc) are common in both obesity and arterial hypertension (AH), and are risk factors for cardiovascular disease and sudden death. METHODS: We compared the frequencies of LVH (ECG criteria) and QTc in obese-AH (n ¼ 41), in normotensive obese (n ¼ 75), in lean-AH (n ¼ 30), and in lean controls (n ¼ 68) comparable for age and sex; in obese patients, LVH and QTc were evaluated under basal conditions and 1 y later, that is, after a significant weight loss induced by bariatric surgery. RESULTS: LVH was more frequent, and QTc was longer, in obese-AH, in normotensive obese, and in lean-AH than in lean controls; after weight loss, frequency of LVH decreased in obese subjects becoming normotensive (n ¼ 87), not in obese subjects remaining hypertensive (n ¼ 29), while QTc decreased in all obese subjects. CONCLUSION: Weight loss can effectively reduce QTc; when concomitant AH disappears, weight loss can also reduce the prevalence of LVH. In obese patients remaining hypertensive, aggressive pharmacological treatment is therefore indicated to correct LVH.