Android obesity is associated with a concomitant reduction of IL-10 and adiponectin levels. However, the antiinflammatory status of obesity might require prolonged periods of energy-restricted diets to revert to normal.

OBJECTIVESWe tested the hypothesis that insulin resistance, per se, contributes to increased platelet activation in obesity, independently of underlying inflammation. BACKGROUND Obesity, insulin resistance, and atherosclerosis are closely linked phenomena associated with low-grade inflammation. Obesity is associated with persistent platelet activation in otherwise healthy women. METHODSWe performed a cross-sectional study in 40 obese and 20 non-obese healthy women using urinary thromboxane metabolite excretion as a non-invasive index of platelet activation. An index of insulin sensitivity, S I , and plasma adiponectin, C-reactive protein (CRP), and CD40 ligand (CD40L) levels were measured. RESULTSObese women had significantly (p Ͻ 0.0001) higher 11-dehydro-thromboxane B 2 (11-dehydro-TXB 2 ) excretion (median 718 vs. 211 pg/mg creatinine), CRP (1.13 vs. 0.48 mg/l), and CD40L levels (4.45 vs. 0.90 ng/ml) than controls. Obese women had lower S I (median 2.51 vs. 5.0 10 4 min Ϫ1 /[U/ml], p Ͻ 0.002) and adiponectin (6.3 vs. 10 g/ml, p Ͻ 0.01) than control subjects. On multiple regression analysis, waist-to-hip ratio (␤ ϭ 0.27, p Ͻ 0.05) and S I (␤ ϭ Ϫ0.72, p Ͻ 0.04) predicted 11-dehydro-TXB 2 excretion rate, independently of adiponectin, CRP, CD40L, and lipid patterns. In order to investigate the cause-effect relationship of these associations, we examined the effects of a 12-week weight loss program or a 3-week pioglitazone treatment on urinary 11-dehydro-TXB 2 in 10 women with impaired S I and visceral obesity. Successful weight loss (0.6 kg loss/week) achieved in 5 subjects was associated with increased S I (ϩ92%) and decreased CD40L (Ϫ27%), CRP (Ϫ37%), and 11-dehydro-TXB 2 (Ϫ53%) (p Ͻ 0.05). Consistently, improvement of insulin sensitivity achieved with pioglitazone significantly decreased urinary 11-dehydro-TXB 2 excretion (Ϫ43%, p Ͻ 0.05) without changes in body weight. CONCLUSIONS Insulin resistance is a major determinant of platelet activation in female obesity. (J Am Coll Cardiol 2006;48:2531-8)

OBJECTIVE: To examine the relationship between 24 h ambulatory blood pressure monitoring and three commonest anthropometric measurements for obesity -body mass index (BMI), waist-to-hip ratio (WHR) and waist circumference (W). DESIGN: Cross-sectional survey among outpatients at the Obesity Research Center. SUBJECTS AND METHODS: Four-hundred and sixty-one overweight or obese subjects, non-diabetic, otherwise healthy, aged 20 -70 y, of either sex, were consecutively recruited. All subjects underwent 24 h ambulatory blood pressure monitoring. The population study was separated in normotensive and hypertensive males and females and the possible risk factors for hypertension (W, WHR, BMI and age) were subdivided into different classes of values. RESULTS: Logistic regression shows that W is the most important anthropometric factor associated with the hypertensive risk. Among males with W!102 cm the odds ratio (OR) for hypertension is three times that of males with W<94 cm using casual BP measure (OR 3.04), nearly four times higher using 24 h BP mean (OR 3.97), and even five times higher using day-time BP mean (OR 5.19). Females with W!88 cm have a risk for hypertension twice that of females with W<80 cm, whatever BP measurement was take (casual, 24 h or day-time). Males with WHR!0.96 and females with WHR!0.86 show significant OR for hypertension only by 24 h BP measurement and by day-time BP measurement. BMI seems to have no significant relationship to hypertensive risk. Age shows a significant relationship to hypertensive risk only considering males aged !55 y and females aged !50 y. CONCLUSION: The waist circumference seems to have a strong association with the risk of hypertension, principally by the ambulatory BP monitoring, when compared with casual BP measurement.

Insulin resistance is associated with a low chronic inflammatory state. In this study we investigated the relationship between impaired insulin sensitivity and selected markers of inflammation and thrombin generation in obese healthy women. We examined 32 healthy obese women (body mass index > or = 28), with normal insulin sensitivity (NIS, n = 14) or impaired insulin sensitivity (n = 18), and 10 nonobese women (body mass index < 25). Impaired insulin sensitivity patients had significantly higher levels of C-reactive protein (CRP), TGF-beta 1, plasminogen activator inhibitor-1 (PAI-1), activated factor VII (VIIa), and prothrombin fragment 1 + 2 (F1 + 2) compared with either control subjects or NIS patients. On the other hand, NIS patients had higher CRP, TGF-beta 1, PAI-1, and factor VIIa, but not F1 + 2, levels than controls. Significant inverse correlations were observed between the insulin sensitivity index and TGF-beta 1, CRP, PAI-1, factor VIIa, and F1 + 2 levels. Moreover, significant direct correlations were noted between TGF-beta 1 and CRP, PAI-1, factor VIIa, and F1 + 2 concentrations. Finally, multiple regressions revealed that TGF-beta 1 and the insulin sensitivity index were independently related to F1 + 2. Our results are the first to document an in vivo relationship between insulin sensitivity and coagulative activation in obesity. The elevated TGF-beta 1 levels detected in the obese population may provide a biochemical link between insulin resistance and an increased risk for cardiovascular disease.

Objective: To study signi®cant factors associated with the risk of hypertension among obese women, with and without a history of weight cycling (WC). Design: Case ± control study. Setting: Obesity Clinic of Chieti University, Italy. Subjects: A group of 258 obese women aged 25 ± 64 y (103 cases with hypertension and 155 controls) were recruited. All obese subjects had the same clinical characteristics, were without a family history for hypertension, were non-smokers, had normal lipidemic pro®les and normal glucose tolerance, were not taking any medication and were otherwise healthy. Intervention: In the weight cycling women, the history of WC was established on the basis of at least ®ve weight losses in the previous 5 y due to dieting, with a weight loss of at least 4.5 kg per cycle. A logistic regression model adjusted for confounding variables such as waist-to-hip ratio (WHR) and weight cycling history parameters was used and the odds ratio (OR) with 95% con®dence intervals was calculated. Results: The risk of hypertension increases in subjects with larger WHR (OR 7.8; 95% CI 3.4 ± 17.9) and with a positive history for WC (OR 4.1; 95% CI 2.4 ± 6.9). Further, in obese patients with WC, the weight cycling index and the sum of the weight regained are also important risk factors for hypertension. Conclusions: These ®ndings could support the hypothesis that it is the combined exposure of central-type obesity and WC that strongly raises the risk of hypertension. Sponsorship: This work has been ®nancially supported by a grant