[What do we know about obesity?]. / Cosa sapere sul problema obesità?

The prevalence of obesity is increasing rapidly in most industrialized countries and it is known that obesity is associated with increased risk of cardiovascular morbidity and mortality. Commonly, obesity is defined by the Body Mass Index (BMI). However, BMI fails to consider body fat distribution. The relationship between the risk of metabolic-cardiovascular diseases and body fat distribution indices, rather than measures of the degree of body fatness as expressed by BMI, has long been recognized. Clinical and epidemiological research has found waist circumference to be the best anthropometric indicator of both total body fat and intra-abdominal fat mass. Android obesity is associated with metabolic syndrome and increased cardiovascular risk through molecular mechanisms possibly linking the metabolic syndrome to hemostatic and vascular abnormalities. Obesity guidelines suggest the need for weight reduction using behavioural change to reduce caloric intake and increasing physical activity. A realistic goal for weight reduction is to reduce body weight by 5% to 10% over a period of 6 to 12 months. Combined intervention of a low calories diet, increased physical activity, and behaviour therapy provides better outcomes for long-term weight reduction and weight maintenance than programs that use only one or two of these modalities. The anorexiant drugs affect neurotransmitters in the brain. The sibutramine has norepinephrine and serotonin effects. Orlistat has a different mechanism of action: the reduction of fat absorption. Recently, the blockade of the endocannabinoid system with rimonabant may be a promising new strategy.

Leptin increase is associated with markers of the hemostatic system in obese healthy women.

BACKGROUND: Leptin, a hormone secreted by the adipose tissue, might be a link between obesity and increased morbidity for cardiovascular disease. Leptin exerts proinflammatory, pro-angiogenic actions by activating a specific receptor (Ob-Rb) which is expressed in human endothelial cells. Thus, a link may exist between leptin expression and endothelial dysfunction. OBJECTIVES: We sought to determine whether in obese women there is a correlation between leptin levels, endothelial perturbation and coagulative activation. METHODS: Circulating levels of leptin, von Willebrand Factor (VWF), factor (F)VIIa, prothrombin fragment 1 + 2 (F1+2), were measured in 51 non-diabetic, obese women and in 51 normal-weight subjects, using immunoenzymatic assays. RESULTS: Obese women had significantly higher levels of leptin, VWF, FVIIa, F1+2 compared with healthy women. Simple correlation coefficients showed significant correlation between leptin and either VWF, FVIIa, or F1+2 concentrations. A multiple linear regression analysis, performed to quantify further the relationship between leptin levels and the above-mentioned variables as well as the inflammatory marker C-reactive protein (CRP) and including age, body mass index (BMI), waist-hip ratio (WHR) and lipid parameters as potential confounders, revealed that only FVIIa and VWF were independently related to leptin levels. Reduction in adipose tissue after weight loss resulted in a decrease in both circulating leptin and endothelial and coagulative activation markers. CONCLUSIONS: We suggest that leptin might have pro-atherogenic effects in vivo, with a mechanism involving endothelial cell activation.