Visceral/epicardial adiposity in nonobese and apparently healthy young adults: Association with the cardiometabolic profile

Objective

We investigate associations of regional adipose tissues with cardiometabolic profile of nonobese and apparently healthy young adults.

Methods

Four hundred twenty-five nonobese and apparently healthy individuals were assessed for blood pressure and fasting lipid profile, blood glucose and adiponectin. Subcutaneous abdominal adipose tissue (SAT) and ectopic fat depots (visceral abdominal adipose tissue [VAT], epicardial adipose tissue [EAT] and hepatic fat fraction [HFF]) were quantified by magnetic resonance imaging.

Results

According to anthropometric measurements, blood pressure and blood markers, the population (18–35 years, 54% women) had a low cardiometabolic risk. Compared to women, men had more VAT, EAT and HFF, but less SAT. Regional adipose tissues were positively correlated with each other. VAT and EAT carried significant correlations with all markers of cardiometabolic risk, while SAT and HFF correlated variably with these markers. While taking into account age and gender, SAT, VAT and EAT were associated with most cardiometabolic markers, while HFF was only associated with total cholesterol/high-density lipoprotein ratio (TC/HDL-C) and triglycerides (TG). When comparing SAT, VAT and EAT head-to-head, VAT was the only adipose tissue location maintaining significant association with most markers of cardiometabolic risk. Greater VAT (≥50th percentile) was associated with a worse cardiometabolic profile, whether individuals were overweight or normal weight.

Conclusion

Even in nonobese and apparently healthy young women and men, accumulation of ectopic visceral adiposity in general, and of VAT in particular, is associated with a worse cardiometabolic profile whether individuals were overweight or normal weight.     

Visceral Adiposity and Left Ventricular Mass and Function in Patients With Aortic Stenosis: The PROGRESSA Study

Background

Recent studies have reported that obesity, metabolic syndrome, and diabetes are associated with left ventricular (LV) hypertrophy (LVH) and dysfunction in patients with aortic stenosis (AS). The purpose of this study was to examine the association between amount and distribution of body fat and LVH and systolic dysfunction in AS patients.

Methods

One hundred twenty-four patients with AS were prospectively recruited in the PROGRESSA (Metabolic Determinants of the Progression of Aortic Stenosis) study and underwent Doppler echocardiography and computed tomography scan. Presence and severity of LVH was assessed according to LV mass indexed for height^2.7 and LV dysfunction according to global longitudinal strain (GLS). Computed tomography was used to quantify abdominal visceral (VAT) and subcutaneous (SAT) adipose tissue, and total adipose tissue (TAT).

Results

Body mass index (BMI) correlated strongly with TAT (r = 0.85), moderately with VAT (r = 0.70), and SAT (r = 0.69), and weakly with the proportion of VAT (VAT/TAT ratio: r = 0.19). In univariate analysis, greater BMI, TAT, VAT, SAT, and VAT/TAT were associated with increased LV mass index and greater VAT and VAT/TAT ratio were associated with reduced GLS. Multivariate analysis revealed that larger BMI (P < 0.0001) and greater VAT/TAT ratio (P = 0.01) were independently associated with higher prevalence of LVH, and only the VAT/TAT ratio (P = 0.03) was independently associated with reduced GLS.

Conclusions

The results of this study suggest that total and visceral adiposity are independently associated with LVH in patients with AS. Furthermore, impairment of LV systolic function does not appear to be influenced by total obesity but is rather related to excess visceral adiposity. These findings provide impetus for elaboration of interventional studies aiming at visceral adiposity in the AS population.     

Predominance of small dense LDL differentiates metabolically unhealthy from metabolically healthy overweight adults in Korea

Objective

The purposes of this study were (1) to determine the association between lipoprotein subfraction profiles and metabolically healthy overweight (MHO) phenotype, as defined by visceral adiposity; and (2) to identify the strongest predictor of metabolic health among the lipoprotein measurements.

Materials/Methods

This cross-sectional study was comprised of 462 overweight patients, who were classified as MHO or non-MHO based on their visceral adipose tissue (VAT) area to subcutaneous adipose tissue area (SAT) ratio (VAT/SAT ratio). Serum lipoprotein subfraction analyses and other metabolic parameters were measured.

Results

Among the overweight participants, two hundred fifty-five individuals (53.7%) had the MHO phenotype. After adjusting for age, sex, medication, lifestyle factors, and confounding metabolic characteristics, the non-MHO group showed significantly higher lipid levels and a greater prevalence of unfavorable lipid profiles. LDL subclass pattern type B was the most significant predictor of the non-MHO phenotype (odds ratio 2.70; 95% CI 1.55–4.69), while serum LDL cholesterol level was not a significant predictor of the non-MHO phenotype.

Conclusions

Lipoprotein subfraction particle measurements were significantly associated with the non-MHO phenotype and a higher VAT/SAT ratio, with small dense LDL predominance being the most significant predictor of MHO phenotype. These findings will help identify MHO and non-MHO phenotypes and perhaps lead to a development of cost-effective individualized treatments.     

Altered pattern of cannabinoid type 1 receptor expression in adipose tissue of dysmetabolic and overweight patients

In overweight patients (OW), the increased peripheral activity of the endocannabinoid system in visceral adipose tissue (VAT) may be mediated by cannabinoid type 1 (CB1) receptor expression. We determined whether CB1 receptor splice variants and messenger RNA (mRNA) levels in perirenal and subcutaneous adipose tissues are associated with obesity and metabolic syndrome (MetS). Gene expression with multiple-primers real-time polymerase chain reaction (TaqMan; Applied Biosystem, Weiterstadt, Germany) was performed to study VAT and paired subcutaneous adipose tissue (SAT) mRNA from 36 consecutive patients undergoing nephrectomy. Cannabinoid type 1A and CB1E mRNAs variants with the longer version of exon 4 were expressed. The CB1 expression in perirenal VAT significantly correlated with body mass index (BMI). Paired subcutaneous/perirenal samples from normal-weight patients (BMI <25 kg/m²) showed higher CB1 expression in SAT (P = .002), whereas in OW (BMI ≥25 kg/m²), the higher CB1 expression was in VAT (P = .038). In unpaired samples, SAT of normal-weight patients had significantly higher CB1 mRNA levels compared with SAT of OW, whereas higher CB1 expression (P = .009) was found in VAT of OW (n = 25). Overweight patients with increased visceral CB1 expression had higher waist circumference (P < .01), insulin (P < .01), and homeostasis model assessment index (P < .01). In addition, patients with the MetS (n = 22) showed higher CB1 expression in perirenal adipose tissues (P = .007). Visceral adipose CB1 expression correlated with BMI. Overweight patients and those with MetS showed a CB1 expression pattern supporting a CB1-mediated overactivity of the endocannabinoid system in human VAT.     

Inhibition of ERK1/2 pathway suppresses adiponectin secretion via accelerating protein degradation by Ubiquitin–proteasome system: Relevance to obesity-related adiponectin decline

Objective

Predominantly secreted by adipose tissue, adiponectin possesses insulin-sensitizing, anti-atherogenic, anti-inflammatory, and anti-angiogenic properties. Paradoxically, obesity is associated with declined plasma adiponectin levels; however, the underlying mechanisms remain elusive. In this study, we investigated the mechanistic involvement of MEK/ERK1/2 pathway in obesity-related adiponectin decrease.

Materials/Methods

C57 BL/6 mice exposed to a high-fat diet (HFD) were employed as animal obesity model. Both fully-differentiated 3T3-L1 and mouse primary adipocytes were used in the in vitro experiments.

Results

Obesity and plasma adiponectin decline induced by prolonged HFD exposure were associated with suppressed ERK1/2 activation in adipose tissue. In adipocytes, specific inhibition of MEK/ERK1/2 pathway decreased intracellular and secretory adiponectin levels, whereas adiponectin gene expression was increased, suggesting that MEK/ERK1/2 inhibition may promote adiponectin protein degradation. Cycloheximide (CHX)-chase assay revealed that MEK/ERK1/2 inhibition accelerated adiponectin protein degradation, which was prevented by MG132, a potent proteasome inhibitor. Immunoprecipitation assay showed that intracellular MEK/ERK1/2 activity was negatively associated with ubiquitinated adiponectin protein levels. Consistently, long-term HFD feeing in mice increased ubiquitinated adiponectin levels in the epididymal fat pads.

Conclusions

Adipose tissue MEK/ERK1/2 activity can differentially regulate adiponectin gene expression and protein abundance and its suppression in obesity may play a mechanistic role in obesity-related plasma adiponectin decline.     

The Relationship of Body Mass and Fat Distribution With Incident Hypertension : Observations From the Dallas Heart Study

Background

Obesity has been linked to the development of hypertension, but whether total adiposity or site-specific fat accumulation underpins this relationship is unclear.

Objectives

This study sought to determine the relationship between adipose tissue distribution and incident hypertension.

Methods

Normotensive participants enrolled in the Dallas Heart Study were followed for a median of 7 years for the development of hypertension (systolic blood pressure [SBP] ≥140 mm Hg, diastolic blood pressure ≥90 mm Hg, or initiation of blood pressure medications). Visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) was quantified by magnetic resonance imaging and proton-spectroscopic imaging, and lower body fat (LBF) was imaged by dual-energy x-ray absorptiometry. Multivariable relative risk regression was performed to test the association between individual fat depots and incident hypertension, adjusting for age, sex, race/ethnicity, diabetes, smoking, SBP, and body mass index (BMI).

Results

Among 903 participants (median age, 40 years; 57% women; 60% nonwhite; median BMI 27.5 kg/m²), 230 (25%) developed incident hypertension. In multivariable analyses, higher BMI was significantly associated with incident hypertension (relative risk: 1.24; 95% confidence interval: 1.12 to 1.36, per 1-SD increase). However, when VAT, SAT, and LBF were added to the model, only VAT remained independently associated with incident hypertension (relative risk: 1.22; 95% confidence interval: 1.06 to 1.39, per 1-SD increase).

Conclusions

Increased visceral adiposity, but not total or subcutaneous adiposity, was robustly associated with incident hypertension. Additional studies will be needed to elucidate the mechanisms behind this association.     

Relationship between vaspin gene expression and abdominal fat distribution of Korean women

Visceral adipose tissue-derived serpin (vaspin) is a novel adipokine that is thought to have insulin-sensitizing effects. We investigated vaspin mRNA expression in abdominal adipose tissue and examined how gene expression related to abdominal fat distribution and metabolic parameters in Korean women. We measured anthropometric variables, metabolic parameters, serum vaspin concentration, and vaspin mRNA expression in abdominal adipose tissue obtained from women who underwent abdominal gynecological surgery and were aged 18-67 years (n = 85). Visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) area were measured in 40 subjects using computed tomography (CT). Vaspin expression was analyzed by real-time quantitative RT-PCR according to abdominal fat distribution. Vaspin mRNA expression was greater in adipocytes than in stroma/vascular cells. In the total subjects, vaspin expression was significantly higher in SAT than in VAT. Vaspin expression in SAT in subcutaneous fat type (VSR ≤ 0.3) was significantly higher than in visceral fat type (VSR > 0.3), although vaspin expression in VAT was similar between subcutaneous and visceral fat type. There was a significant negative correlation between vaspin expression in SAT and VAT area (r = -0.55, p = 0.001). Serum vaspin concentration was significantly correlated with fasting insulin (r = 0.30, p = 0.02), HOMA-IR (r = 0.29, p = 0.02), and the ratio of vaspin expression in VAT to vaspin expression in SAT (r = 0.41, p = 0.04). Vaspin expression in abdominal adipose tissue was adipocyte-specific and vaspin expression in SAT decreased as VAT area increased.     

Reduced plasma visfatin/pre-B cell colony-enhancing factor in obesity is not related to insulin resistance in humans

CONTEXT: Visfatin was recently identified as a protein highly expressed and secreted in adipose tissue with insulin-mimetic effect and is a candidate hormone to help explain the association among adipose tissue expansion, insulin resistance, and type 2 diabetes. OBJECTIVE: The objective of the study was to assess expression of visfatin in lean and obese subjects and in sc and visceral adipose tissue and moreover to explore the role of visfatin on insulin resistance in humans. DESIGN: We measured circulating visfatin and its mRNA expression in sc adipose tissue (SAT) in lean and obese subjects. Furthermore, we measured visfatin mRNA in visceral adipose (VAT) and SAT by quantitative RT-PCR. Finally, plasma visfatin and its mRNA in SAT were measured under free fatty acid-induced insulin resistance in healthy subjects. RESULTS: Plasma visfatin and its mRNA in SAT were significantly lower in obese subjects, compared with normal-weight controls. Both circulating visfatin and SAT visfatin mRNA were negatively correlated with body mass index, whereas no correlation was found with homeostasis model assessment. Significantly higher visfatin mRNA was found in VAT of obese subjects, compared with lean controls. Interestingly, visfatin mRNA in VAT was positively correlated with BMI. Elevation of free fatty acid induced a condition of insulin resistance but did not affect either circulating visfatin or its mRNA. CONCLUSIONS: Our findings show that, in human obesity, plasma visfatin is reduced, whereas visfatin mRNA is differentially regulated in SAT and VAT. Visfatin is not related to insulin resistance either as assessed by homeostasis model assessment or during lipid infusion.     

Type 2 diabetes and metabolic syndrome are associated with increased expression of 11beta-hydroxysteroid dehydrogenase 1 in obese subjects

OBJECTIVE: The role of glucocorticoids production in adipose tissue in the development of metabolic disorders in humans has not been fully characterized. We investigated whether in obese subjects, 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) expression in subcutaneous (SAT) and visceral (VAT) adipose tissue is associated with the occurrence of metabolic disorders and the expression of adiponectin and tumor necrosis factor alpha (TNFalpha) and two glucocorticoid-regulated adipokines able to influence the metabolic control. DESIGN AND SUBJECTS: Sixty-two obese patients were enrolled in the study. SAT and VAT samples were obtained from 13 patients undergoing bariatric surgery (body mass index (BMI) 39.1+/-5.3 kg/m(2)). SAT samples were obtained from 49 patients who underwent periumbilical biopsy (BMI 36.9+/-5.1 kg/m(2)). MEASUREMENTS: Oral glucose tolerance tests in subjects without known diabetes. Circulating glucose, lipid, insulin, adiponectin, TNFalpha and urinary-free cortisol levels. Real-time PCR to quantify mRNA levels of 11beta-HSD1, hexose-6-phosphate dehydrogenase (H6PDH), adiponectin and TNFalpha. Western blot analysis to evaluate 11beta-HSD1 protein expression. RESULTS: In the majority of the obese subjects, VAT expresses more 11beta-HSD1 than SAT. VAT 11beta-HSD1 expression was not associated with metabolic disorders. SAT 11beta-HSD1 mRNA levels were higher in subjects with than in those without metabolic syndrome (P<0.05) and in patients with type 2 diabetes compared to patients with impaired or normal glucose tolerance (P<0.0001). SAT 11beta-HSD1 expression was independently related to fasting glucose (P<0.0001) and urinary-free cortisol levels (P<0.01), and increased expression of 11beta-HSD1 was associated with increased adiponectin and TNFalpha expression and decreased serum adiponectin levels (all P's <0.05). CONCLUSIONS: In obese subjects, increased 11beta-HSD1 expression in SAT, but not in VAT, is associated with the worsening of metabolic conditions. We hypothesize that higher glucocorticoid production in adipose tissue would favor the development of metabolic disorders through a decrease in adiponectin release.     

Glucocorticoid metabolism within superficial subcutaneous rather than visceral adipose tissue is associated with features of the metabolic syndrome in South African women

OBJECTIVE: Glucocorticoid hyperactivity in adipose tissue, due to up-regulation of local glucocorticoid reactivation by 11beta-hydroxysteroid dehydrogenase-1 (11HSD1) or of glucocorticoid receptors (GR), may underpin susceptibility to the metabolic syndrome. This hypothesis has been tested extensively in subcutaneous adipose tissue (SAT) but inadequately in visceral adipose tissue (VAT). The aim of the study was therefore to examine expression of 11HSD1, GRalpha and hexose-6-phosphate dehydrogenase (H6PDH), which supplies cofactor for 11HSD1, in abdominal adipose tissue compartments and to characterize their relation to metabolic syndrome parameters. DESIGN AND SUBJECTS: A cross-sectional study including 26 premenopausal South African women. MEASUREMENTS: Biopsies were taken for measurement of mRNA levels by real-time polymerase chain reaction (RT-PCR) and 11HSD1 activity from VAT, and deep and superficial SAT compartments during elective surgery. Prior to surgery, blood pressure, blood lipid profile, body composition [by dual X-ray absorptiometry (DEXA) scan], body fat distribution [by computed tomography (CT) scan], and glucose tolerance were determined. RESULTS: 11HSD1 activity (P < 0.01) was higher in VAT than SAT, but 11HSD1 and GRalpha mRNA levels were not statistically different between compartments. 11HSD1 mRNA levels in superficial SAT correlated with VAT volume (R = 0.57, P < 0.01), insulin sensitivity calculated from the oral glucose tolerance test (OGTT) (R = -0.52, P < 0.016) and blood pressure (R = 0.48, P < 0.016). Apart from a correlation between deep SAT 11HSD1 activity and blood pressure (R = 0.72, P < 0.01), glucocorticoid action in deep SAT and VAT depots was not significantly associated with any metabolic syndrome parameters. CONCLUSION: Increased capacity for glucocorticoid regeneration in superficial SAT but not VAT is associated with visceral adiposity and other features of the metabolic syndrome in women.     

Markers of endothelial cell dysfunction are increased in human omental adipose tissue from women with pre-existing maternal obesity and gestational diabetes

Objective

To determine the effect of maternal obesity and gestational diabetes mellitus (GDM) on the expression and release of genes involved in endothelial cell dysfunction in human placenta and omental adipose tissue.

Materials/Methods

Human placenta and omental adipose tissue were obtained from non-obese and obese normal glucose tolerant (NGT) women and women with GDM at the time of Caesarean section. Quantitative RT-PCR was performed to determine the level of expression. Tissue explants were performed to determine the release of proteins of interest.

Results

There was no effect of pre-existing maternal obesity or GDM on placental gene expression or secretion of members of the VEGF family members (PLGF and VEGF-A expression and secretion; sFlt-1 release; VEGFR1 and VEGFR2 mRNA expression); FGFR1 mRNA expression, FGF2 mRNA expression and secretion; endoglin mRNA expression and secretion (sEng); and the adhesion molecules ICAM-1 and VCAM-1. On the other hand, in omental adipose tissue, pre-existing maternal obesity and GDM were associated with increased gene expression of PLGF, endoglin and ICAM-1 and increased secretion of PLGF, sFlt-1, FGF2, sEng and sICAM-1. There was, however, no effect of maternal pre-existing obesity and GDM on VEGF-A, VEGFR1, VEGFR2, FGFR1 and VCAM-1 expression or secretion.

Conclusions

This study demonstrated the presence of abnormal expression and secretion of angiogenic proteins and adhesion molecules in omental adipose tissue, but not placenta, from pregnant women with GDM and pre-existing maternal obesity. Increased angiogenic and adhesion molecules released from adipose tissue may affect angiogenesis, inflammation and or lipid and glucose metabolism in both mum and her offspring.     

Association of Visceral and Subcutaneous Adiposity with Kidney Function

Background and objectives: Obesity is a risk factor for incident chronic kidney disease (CKD). Visceral (VAT) and subcutaneous adipose tissue (SAT) may confer differential metabolic risk profiles. The relations of VAT and SAT were analyzed with CKD as estimated by creatinine- and cystatin-based estimating equations.Design, setting, participants, & measurements: Participants from the Framingham Offspring Study who underwent abdominal computed tomography for VAT and SAT quantification were included (n = 1299; 53% women; mean age 60 yr). CKD was defined as estimated GFR <60 ml/min per 1.73 m², as estimated using creatinine (n = 89) in the Modification of Diet in Renal Disease (MDRD) formula or by cystatin C (n = 136). Regression models evaluated the cross-sectional relations between VAT and SAT with CKD and cystatin C, with age and gender adjustment and cardiovascular risk factor adjustment.Results: Neither VAT nor SAT was associated with CKD as estimated by the MDRD equation. In contrast, both VAT and SAT were associated with CKD when defined using cystatin-based equations. The estimated decrease in estimated GFR by cystatin C per 1-SD increase of VAT was 1.9 ml/min per 1.73 m² and for SAT was 2.6 ml/min per 1.73 m² in a multivariable-adjusted model.Conclusions: VAT and SAT were associated with CKD when defined using cystatin C estimating equations but not when using a creatinine-based estimating equation. Mechanisms linking adipose tissue to cystatin C warrant further research.Chronic kidney disease (CKD) is common and affects 13.1% of adults in the United States and continues to increase (1). As a consequence of CKD, risk for all-cause and cardiovascular mortality is increased (2). Obesity is a risk factor for CKD, although the mechanisms are poorly understood (3,4). Given the current epidemic of obesity (5), it is important to understand potential mechanisms that link obesity to CKD.Several studies have suggested that visceral adiposity, as measured by computed tomography (CT) scan, may be a better predictor of cardiovascular disease (CVD) risk factors as compared with traditional clinical anthropometric measures such as body mass index (BMI) and waist circumference (6–8). Whereas clinical anthropometric measures offer easily obtainable measures of central adiposity, they do not allow for the differentiation between subcutaneous and visceral fat. One previous study suggested that central obesity as estimated by waist-to-hip ratio was inversely associated with level of kidney function (9). Because of the inability of waist-to-hip ratio to detect subcutaneous as compared with visceral fat, it is uncertain whether there is a differential association between abdominal fat compartments and kidney function.Given the previous literature suggesting strong associations between metabolic risk factors with both visceral fat and CKD, we hypothesized that community-dwelling individuals with more visceral abdominal adiposity would be more likely to have CKD, using creatinine-based estimating equations. We also sought to relate cystatin C, a novel marker of kidney function, and cystatin C–based estimation of GFR to visceral (VAT) and subcutaneous adipose tissue (SAT).     

La grasa epicárdica se relaciona con la visceral,el síndrome metabólico y la resistencia a la insulina en mujeres menopáusicas

Introduction and objectives

Epicardial adipose tissue has been associated with several obesity-related parameters and with insulin resistance. Echocardiographic assessment of this tissue is an easy and reliable marker of cardiometabolic risk. However, there are insufficient studies on the relationship between epicardial fat and insulin resistance during the postmenopausal period, when cardiovascular risk increases in women. The objective of this study was to examine the association between epicardial adipose tissue and visceral adipose tissue, waist circumference, body mass index, and insulin resistance in postmenopausal women.

Methods

A cross sectional study was conducted in 34 postmenopausal women with and without metabolic syndrome. All participants underwent a transthoracic echocardiogram and body composition analysis.

Results

A positive correlation was observed between epicardial fat and visceral adipose tissue, body mass index, and waist circumference. The values of these correlations of epicardial fat thickness overlying the aorta-right ventricle were r = 0.505 (P < .003), r = 0.545 (P < .001), and r = 0.515 (P < .003), respectively. Epicardial adipose tissue was higher in postmenopausal women with metabolic syndrome than in those without this syndrome (mean [standard deviation], 544.2 [122.9] vs 363.6 [162.3] mm ²; P = .03).

Conclusions

Epicardial fat thickness measured by echocardiography was associated with visceral adipose tissue and other obesity parameters. Epicardial adipose tissue was higher in postmenopausal women with metabolic syndrome. Therefore, echocardiographic assessment of epicardial fat may be a simple and reliable marker of cardiovascular risk in postmenopausal women.Full English text available from:www.revespcardiol.org/en     

Relationship between serum adiponectin and leptin concentrations and body fat distribution

The aim of this study was to investigate the relationship between adiponectin and leptin and body fat distribution. One hundred and ninety-seven women participated in this study. Subjects were grouped based on their visceral adipose tissue area (VAT). Body fat distribution was determined by computed tomography. The numbers in the subcutaneous fat dominant group (SFDG) and visceral fat dominant group (VFDG) were 79 and 118, respectively. The VFDG showed lower adiponectin levels than the SFDG (8.9+/-0.4 microg/ml versus 11.4+/-0.7 microg/ml, P=0.006), but leptin levels did not differ significantly between groups (18.8+/-1.1 ng/ml versus 17.7+/-1.8 ng/ml, P=0.111). Adiponectin levels were inversely correlated with fasting insulin, HOMA-IR, triglyceride, SBP and DBP, subcutaneous adipose tissue area (SAT) and VAT, and waist-to-hip ratio (WHR). Leptin levels were positively correlated with fasting glucose and insulin, HOMA-IR, triglyceride, SBP and DBP, VAT and SAT, and WHR (all values of P<0.05). VAT and HDL-cholesterol were independent variables of adiponectin concentrations (R(2)=0.207, P<0.0001), and SAT, fasting insulin, and HOMA-IR were independent variables of leptin concentrations (R(2)=0.498, P<0.0001) In conclusion, adiponectin and leptin concentrations, although associated with metabolic parameters, were more strongly influenced by VAT in the case of adiponectin, and by SAT in the case of leptin.     

Abdominal adiposity depots are correlates of adverse cardiometabolic risk factors in Caucasian and African-American adults

Objective:

Accumulation of adipose tissue is associated with cardiometabolic risks. Although visceral adipose tissue (VAT) has been strongly implicated in this relationship, there is still some debate regarding the contribution of abdominal subcutaneous adipose tissue (SAT). The purpose of this study was to determine the contribution of abdominal SAT to cardiometabolic risk factors, independent of total and visceral adiposity. These relationships were assessed in Caucasian and African Americans.

Design:

It is a cross-sectional analysis of the Pennington Center Longitudinal Study.

Subjects:

Data were extracted from 1246 participants. Total body fat mass (FM) was measured by dual-energy X-ray absorptiometry, whereas abdominal VAT and SAT areas (cm²) were measured with computed tomography. The cardiometabolic risk factors included resting blood pressure (BP), fasting blood glucose and triglyceride concentrations and high-density lipoprotein cholesterol (HDL-C).

Results:

Positive relationships across tertiles of VAT were seen for the participants with high glucose, high BP and low HDL-C (P<0.043). There was also a significant increase in the percentage of participants with two or more cardiometabolic risk factors across most tertiles of abdominal SAT (P<0.042). Logistic regression analysis showed that in univariate models, all adiposity measures were significantly associated with increased odds of having all risk factors in men and women. In multivariate models, VAT was significantly associated with most risk factors across gender. Abdominal SAT and FM (odds ratios (ORs) 1.3–2.1; all P<0.05) were associated with fewer risk factors after accounting for VAT. VAT (OR=5.9 and 5.3) and SAT (OR=2.0 and 1.8) were both associated with higher odds of the presence of two or more cardiometabolic risk factors in both males and females (P<0.001).

Conclusion:

The data suggest that abdominal SAT is not protective against unfavorable cardiometabolic risk profiles. These conclusions were consistent across ethnic groups.     

Metabolic syndrome associates with left atrial dysfunction

Background and aims

Obesity and metabolic syndrome (MetS) are risk factors of atrial fibrillation (AF), but limited data exist on their effect on left atrial (LA) function. The aim of the study was to evaluate the effects of cardiac, hepatic and intra-abdominal ectopic fat depots and cardiometabolic risk factors on LA function in non-diabetic male subjects.

The gene expression of CTRP12 but not CTRP13 is upregulated in both visceral and subcutaneous adipose tissue of obese subjects

Obesity is a well-known chronic low-grade inflammation condition characterized by dysregulated adipokine secretion and function. Both CTRP12 and CTRP13 are adipokines that influence glucose and lipid metabolism. We aimed to investigate CTRP12, CTRP13, and inflammatory gene expressions in subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) from obese women who underwent bariatric surgery in comparison with the normal weight women. This case-control study included 20 obese [body mass index (BMI) > 35–40 kg/m²] candidates for bariatric surgery and 20 normal-weight women (BMI <25 kg/m²) as control group, who underwent elective surgeries. Real-time PCR was used to evaluate mRNA expression levels of CTRP12, CTRP13, and inflammatory genes in SAT and VAT from both groups. We observed significantly higher mRNA expression of CTRP12 in SAT (p = 0.048) and VAT (p = 0.046) from obese patients compared to the controls. There was significantly greater expression of IL-6 and MCP-1 inflammatory genes in SAT (p = 0.013 and p = 0.005 respectively) and VAT (p = 0.000 and p = 0.001 respectively) of obese patients compared to the control group. IL-1β (p = 0.015) and TNF-α (p = 0.014) expressions significantly increased in VAT from obese patients compared to the control group. Spearman correlation analysis showed that CTRP12 expression significantly correlated with obesity indices. Our findings showed that CTRP12 significantly increased in both VAT and SAT of obese group. More importantly, we observed a positive correlation between CTRP12 with inflammatory parameters. These results indicated that CTRP12 might be part of an intricate network for glucose metabolism and obesity-related inflammation processes.