Increased visceral adipose tissue rather than BMI as a risk factor for dementia

In addition to the association between overweight/obesity and cardiovascular disorders, with the presence of a vascular burden as a cofactor, recent studies have particularly focused on the association between indicators of adiposity and dementia. Particularly, renewed predictive value has been addressed to body mass index (BMI). A high BMI can increase the risk for dementia when measured before clinical dementia onset. Although the use of BMI in population-based and clinical studies is feasible, this is an index of weight excess and shows limits in its ability to distinguish between fat and fat-free mass or between deep (visceral) abdominal fat and subcutaneous abdominal fat. In this scenario, we suggest that visceral adipose tissue (VAT) rather than BMI should be considered as a concurrent factor in the development of dementia. Several physiopathologic theories (neurochemical, hormonal, atherosclerotic and inflammatory) have been proposed to explain the decline of cognitive functions. Along with this, well known cardiovascular risk factors (dyslipidaernia, insulin resistance, blood pressure, adipocytokine/chemokines, atherosclerosis) contributing to the development of cognitive decline seem more strongly related to body fat distribution, particularly visceral adipose tissue (VAT), rather than to BMI. With this regard, VAT may be reasonably considered to play a predominant role

Regulated on activation, normal-T cell expressed and secreted (RANTES/CCL5) levels: an association with epicardial visceral fat thickness

Introduction: Epicardial adipose tissue (EAT), accumulated around the heart, is considered an index of visceral adiposity and a promising indicator of high cardio-metabolic risk. Evidences showing that EAT is a metabolically active organ and a source of inflammatory adipo-chemocytokines suggest a condition of chronic inflammation in this small cardiac fat depot. However, the potential links between cardiac adiposity and circulating levels of inflammatory adipo-chemokines, as markers of subclinical inflammation, are not completely understood. Our aim is to evaluate whether cardiac adiposity, measured as EAT thickness, is related to Regulated on activation, Normal T Cell Expressed and Secreted (RANTES/CCL5) levels, in obese patients. Methods: EAT thickness (meauserd by echocardiography, on the free wall of right ventricle), RANTES/CCL5 and other inflammatory markers (by ELISA kit) were measured in 36 women with uncomplicated obesity (OB) (BMI 41.6\ub15.6 kg/m2) and 15 normal-weight controls. Abdominal visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) were assessed by computed tomography (CT). Results: OB patients had thicker EAT (6.8\ub10.9 vs. 1.3\ub10.3 mm, p<0.0001) (Fig.1) and higher RANTES/CCL5 levels (2468.9\ub1745.5 vs. 1272.1\ub1413.7 pg/ml, p<0.03) than controls (Fig. 2). The EAT thickness positively correlated with RANTES/CCL5 concentrations (r2=0.65, p<0.001) (Fig.3). Moreover, EAT thickness and RANTES/CCL5 concentration were directly correlated with indices of fat distribution (VAT, VAT/SAT and waist, p<0.001 for all). Notably, when using multiple regression analysis, RANTES/CCL5 levels most closely correlated with EAT thickness (t=3.93) and VAT areas (t=3.77), while other indices of fat distribution did not enter the model. Conclusions: EAT thickness, an indicator of cardiac adiposity, may be related to inflammatory adipo-chemokines in visceral-obese patients and might be used as a reliable marker of visceral adiposity. The elevated RANTES/CCL5 levels, contributing to the pro-inflammatory state, may also lead to cardio-metabolic disorders

L'utilit\ue0 dell'oral glucose tolerance test nella diagnosi di diabete mellito

Diagnostic criteria for diabetes mellitus from fasting glycemia introduced on 1997 by the American Diabetes Association (ADA) modified the prevalence of diabetes, as well as that of prediabetes which were previously based on the oral glucose tolerance test (OGTT). In the following years a lot of trials agreed in demonstrating that the only baseline blood glucose would result in underestimation of diabetes, even in a relevant manner. At the same time the two classes defined as "impaired fasting glucose" (IFG) by means of fasting glycemia and as "impaired glucose tolerance" (IGT) by OGTT proved to not overlap. IGT was more sensitive in predicting the appearance of diabetes, the overall mortality from any cause and that due to cardiovascular disease. All the above mentioned evidences led the ADA to modify on 2003 the previously suggested diagnostic criteria. The cut-off value of baseline glycemia was lowered from 110 to 100 mg/dl and the values under 100 mg/dl are to be considered as normal. However this caused the inclusion in prediabetes millions of subjects who were considered healthy by the previous classification. An open problem is the underestimation of the prevalence of diabetes, as after 1997 ADA did not modify the baseline glycemic cut-off level. Up to now the OGTT maintains its usefulness in the diagnosis of diabetes mellitus, as a higher diagnostic sensitivity when compared to fasting glycemia has been clearly demonstrated

Epicardial fat : from the biomolecular aspects to the clinical practice

Epicardial fat is the visceral fat depot of heart. It is a metabolically active organ with anatomical and functional contiguity to the myocardium. A dichotomous role has been attributed to the epicardial fat. Under physiological conditions, epicardial fat displays biochemical and thermogenic cardio-protective properties. Under pathological circumstances epicardial fat can locally affect the heart and coronary arteries through vasocrine or paracrine secretion of pro-inflammatory cytokines. Epicardial fat can be measured with imaging techniques. Epicardial fat thickness reflects intra-abdominal and myocardial fat and correlates with metabolic syndrome and coronary artery disease. Epicardial fat measurement may play a role in the stratification of the cardio-metabolic risk and serve as therapeutic target. Weight loss and anti-inflammatory drugs targeting the fat may modulate epicardial fat. Because epicardial and myocardial tissues share the same coronary arterial supply it is reasonable to hypothesize that improved local vascularisation may resume epicardial fat to its physiological role