Metabolic syndrome (MetS) represents a combination of cardiometabolic risk factors, including visceral obesity, glucose intolerance or type 2 diabetes, elevated triglycerides, reduced HDL cholesterol, and hypertension. MetS is rapidly increasing in prevalence worldwide as a consequence of the “epidemic” obesity, with a considerable impact on the global incidence of cardiovascular disease and type 2 diabetes. At present, there is a growing interest on the role of visceral fat accumulation in the occurrence of MetS. In this review, the effects of adipocytokines and other proinflammatory factors produced by fat accumulation on the occurrence of the MetS have been also emphasized. Accordingly, the “hypoadiponectinemia” has been proposed as the most interesting new hypothesis to explain the pathophysiology of MetS.

In this review, we have analyzed the role of visceral obesity in the occurrence of metabolic syndrome (MetS). MetS is a common metabolic disorder that has been related recently to the increasing prevalence of obesity. The disorder is defined in various ways, but in the near future a new definition(s) should be applicable worldwide. The pathophysiology has been largely attributed, in the past years, to insulin resistance, although several epidemiological and pathophysiological data now indicate visceral obesity as a main factor in the occurrence of all the components of MetS. In view of this, relationships among visceral obesity, free fatty acids, dyslipidemia and insulin resistance have been reported. In addition, the effects of some adipocytokines and other proinflammatory factors produced by fat accumulation on the occurrence of MetS have been also emphasized. Accordingly, the "hypoadiponectinemia hypothesis" has been proposed as the most interesting to explain the pathophysiology of MetS. The epidemiologic, pathophysiologic and clinical data reported seem to indicate that MetS might be considered a fatal consequence of visceral obesity.

The authors evaluated the retrieval power of PubMed "Clinical Queries," narrow search string, about therapy in comparison with a modified search string to avoid possible retrieval bias. PubMed search strategy was compared to a slightly modified string that included the Britannic English term "randomised." The authors tested the two strings joined onto each of four terms concerning topics of broad interest: hypertension, hepatitis, diabetes, and heart failure. In particular, precision was computed for not-indexed citations. The added word "randomised" improved total citation retrieval in any case. Total retrieval gain for not-indexed citations ranged from 11.1% to 21.4%. A significant number of Randomized Controlled Trial(s) (RCT)s (9.1-18.2%) was retrieved for each of the selected topics. They were often recently published RCTs. The authors think that correction of the Clinical Queries filter (when they focus on therapy and use narrow searches) is necessary to avoid biased search results with loss of relevant and up-to-date scientifically sound information.

Our data suggest that education may be considered the best predictor of global cardiovascular risk in hypertensives and thus has to be evaluated in the strategies of hypertension and cardiovascular risk management.

This study has been designed to evaluate the impact of adiponectin levels on left ventricular geometry and function in visceral obesity-associated hypertension. 94 consecutive subjects, 53 of them were hypertensives and 41 normotensives with age ≤ 65 years, subgrouped according to the presence or absence of visceral obesity, were studied. Total adiponectin levels were measured by a validated competitive radioimmunoassay. Left ventricular telediastolic internal diameter, interventricular septum, posterior wall thickness, total left ventricular mass (LVM) and normalized for height to the 2.7 power (LVM/h(2.7)), relative wall thickness, left ventricular ejection fraction by echocardiography and isovolumic relaxation time, E/A ratio and deceleration time of E velocity, by pulsed-wave Doppler, were calculated. Plasma adiponectin levels were significantly lower in visceral obesity-associated hypertensives than lean hypertensives (p < 0.001) and in lean normotensives (p < 0.001). LVM and LVM/h(2.7) were significantly (p < 0.05) higher in both hypertensive groups, and in visceral obesity-associated normotensives in comparison with lean normotensives. Adiponectin levels correlated inversely with LVM/h(2.7) but only in normotensives (adjusted R squared 0.77, p < 0.0001) and hypertensives (0.67, p < 0.0001) subjects with visceral obesity. Multiple regression analysis indicated that adiponectin levels remain significantly associated (p < 0.001) to LVM/h(2.7) also when adjusted for age, gender, body mass index, waist to hip ratio and mean blood pressure. Our data suggest an important role of adiponectin in increased LVM/h(2.7) in visceral obesity-associated normotensive and hypertensive subjects. In this last group, adiponectin, more than blood pressure, may be able to explain the development of cardiac damage.