Metabolic syndrome is related to multiple cardiovascular risk factors. Visceral adipose tissue (VAT) plays a key role in metabolic syndrome. Easy detection of VAT could be an important tool to increase knowledge of metabolic syndrome. The objective of this study was to study the relationship of echocardiographic epicardial adipose tissue to anthropometric and clinical parameters of metabolic syndrome. We selected 72 consecutive subjects, 46.5 ؎ 17. M ETABOLIC SYNDROME IS related to multiple cardiovascular risk factors (1-3). There are no wellaccepted criteria for the diagnosis of metabolic syndrome. Nevertheless, it is identified by the presence of three or more metabolic alterations, such as abdominal obesity, hypertension, impaired fasting glucose or glucose intolerance, high levels of triglycerides, low levels of high-density lipoprotein cholesterol, and insulin resistance (4). Plasma adiponectin and C-reactive protein (CRP) have also been proposed to be related to central adiposity and cardiovascular risk (5-7).Visceral obesity seems to play a key role in the development of all features of metabolic syndrome (8 -15). Hence, detection of visceral adipose tissue (VAT), the fat deposited around the internal organs, might be important for risk stratification of metabolic syndrome. Nevertheless, it is difficult to obtain an accurate measurement and characterization of VAT. Several methods are applied as surrogates for estimation of VAT. Anthropometric measurements are the most used, but are frequently imprecise. However, waist circumference is widely accepted as a good predictor of intraabdominal fat mass (16, 17). Imaging techniques are certainly more precise and reliable than anthropometric measurements. Magnetic resonance imaging (MRI), the gold standard technique, estimates VAT accurately, but unfortunately it is costly (18). Recently, we have proposed and validated a new method to estimate VAT by echocardiographic epicardial adipose tissue measurement (19). Epicardial adipose tissue is a true visceral fat deposited around the heart with characteristics of a high insulin-resistant tissue. Epicardial adipose tissue measurement could be an important tool to increase knowledge of metabolic syndrome on epidemiological basis.The aim of this work was to study the relationship of echocardiographic epicardial adipose tissue to anthropometric, metabolic, and cardiac parameters of metabolic syndrome. Subjects and Methods SubjectsWe selected 72 consecutive subjects (Caucasian; 36 females and 36 males), 46.5 Ϯ 17.4 yr of age, with a body mass index (BMI) between 22 and 47 kg/m 2 (median, 34). Echocardiographic measurements were performed in all subjects during routine examinations. Metabolic syndrome was identified by the presence of three or more of the following parameters: BMI greater than 30 kg/m 2 , predominant truncal/abdominal fat distribution (value of waist circumference Ͼ88 cm in women and Ͼ102 cm in men), impaired fasting glucose (fasting glucose Ͼ110 mg/ dl), hypertension (systolic arterial blood pressure Ͼ13...
IACOBELLIS,GIANLUCA, MARIA CRISTINA RIBAUDO, GAETANO LETO, ALESSANDRA ZAPPATERRENO, ELIO VECCI, UMBERTO DI MARIO, AND FRIDA LEONETTI. Influence of excess fat on cardiac morphology and function: echocardiographic study in uncomplicated obesity. Obes Res. 2002;10:767-773. Objective: To evaluate whether or not "uncomplicated" obesity (without associated comorbidities) is really associated with cardiac abnormalities. Research Methods and Procedures:We evaluated cardiac parameters in obese subjects with long-term obesity, normal glucose tolerance, normal blood pressure, and regular plasma lipids. We selected 75 obese patients [body mass index (BMI) Ͼ30 kg/m 2 ], who included 58 women and 17 men (mean age, 33.7 Ϯ 11.9 years; BMI, 37.8 Ϯ 5.5 kg/m 2 ) with a Ն10-year history of excess fat, and 60 age-matched normal-weight controls, who included 47 women and 13 men (mean age, 32.7 Ϯ 10.4 years; BMI, 23.1 Ϯ 1.4 kg/m 2 ). Each subject underwent an oral glucose tolerance test to exclude impaired glucose tolerance or diabetes mellitus, bioelectrical impedance analysis to calculate fat mass and fat-free mass, and echocardiography. Results: Obese patients presented diastolic function impairment, hyperkinetic systole, and greater aortic root and left atrium compared with normal subjects. No statistically significant differences between obese subjects and normal subjects were found in indexed left ventricular mass (LVM/ body surface area, LVM/height 2.7 , and LVM/fat-free mass kg ), and no changes in left ventricular geometry were observed. No statistically significant differences in cardiac parameters between extreme (BMI Ͼ 40 kg/m 2 ) and mild obesity (BMI Ͻ 35 kg/m 2 ) were observed. Discussion:In conclusion, our data showed that obesity, in the absence of glucose intolerance, hypertension, and dyslipidemia, seems to be associated only with an impairment of diastolic function and hyperkinetic systole, and not with left ventricular hypertrophy.
IACOBELLIS, GIANLUCA, MARIA CRISTINA RIBAUDO, ALESSANDRA ZAPPATERRENO, ELIO VECCI, CLAUDIO TIBERTI, UMBERTO DI MARIO, AND FRIDA LEONETTI. Relationship of insulin sensitivity and left ventricular mass in uncomplicated obesity. Obes Res. 2003;11:518-524. Objective: We studied uncomplicated obesity as a model to evaluate the influence of insulin sensitivity per se on left ventricular mass (LVM) and geometry. Research Methods and Procedures:We selected 50 obese subjects (BMI Ͼ 30 kg/m 2 ; 38 women and 12 men; mean age, 38.4 Ϯ 10 years; BMI, 36.4 Ϯ 10.5 kg/m 2 ) with normal blood pressure, glucose tolerance, and plasmatic lipid levels. Thirty lean subjects formed the control group. Each subject underwent euglycemic insulin clamp (7 pmol/min per kg) to evaluate whole body glucose use (M index) and echocardiogram to calculate LVM and indexed LVM. Results: Insulin-resistant obese subjects had higher LVM, LVM/h 2.7 , LVM/body surface area, and LVM/fat-free mass kg (p ϭ 0.001; p ϭ Ͻ0.001 p ϭ 0.001, and p ϭ 0.04, respectively) than obese subjects with normal insulin sensitivity. Multivariate regression analysis showed that M index was the strongest independent correlate of LVM (r 2 ϭ 0.34; p ϭ 0.03). Discussion: Our findings showed that insulin resistance, in uncomplicated obesity, is associated with an increased LVM and precocious changes of left ventricular geometry, whereas preserved insulin sensitivity is not associated with increased LVM.
Several genetic variants of peroxisome proliferator-activated receptor-c2 (PPAR-c2) have been identified, among which Pro12Ala, a missense mutation in exon 2, is highly prevalent in Caucasian populations. Up to now, conflicting results with regard to the association between this mutation and complex traits, such as obesity, insulin sensitivity and Type 2 diabetes, have been reported. We investigated the influence of the Pro12Ala polymorphism of PPAR-c2 on insulin sensitivity in a large Italian population sample, n ¼ 1215, in whom extensive clinical and biochemical analyses were performed. To estimate the insulin sensitivity status, the homeostasis model assessment of insulin resistance (HOMA-IR) was calculated; in the obese/ overweight subjects an oral glucose tolerance test (OGTT) was also performed and the Matsuda insulin sensitivity index (ISI) calculated. The insulin secretion index (homeostasis model assessment of percent b-cell function, HOMA-b%) was utilized to evaluate b-cell function. The effect of the Pro12Ala polymorphism on quantitative variables was tested using multiple linear regression analysis. X12Ala (either Pro12Ala or Ala12Ala) genotype was associated with significantly lower fasting insulin levels compared to Pro/Pro (P ¼ 0.01 after correction for multiple comparisons) in all subjects. Consistent with this finding, significantly lower HOMA-IR was observed in X12Ala carriers (P ¼ 0.013 after correction for multiple comparisons) in all cohort. Moreover, no significant interaction effect was observed between body mass index and X12Ala polymorphism and between gender and X12Ala polymorphism in modulating insulin sensitivity. Our observations substantially extend previous findings and demonstrated that X12Ala variant is significantly associated with greater insulin sensitivity.
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