scholarly journals Central Obesity and Visceral Adipose Tissue Are Not Associated With Incident Atherosclerotic Cardiovascular Disease Events in Older Men

Author(s):  
John T. Schousboe ◽  
Allyson M. Kats ◽  
Lisa Langsetmo ◽  
Tien N. Vo ◽  
Brent C. Taylor ◽  
...  
2016 ◽  
Vol 40 (8) ◽  
pp. 1325-1328 ◽  
Author(s):  
A S Cheung ◽  
C de Rooy ◽  
R Hoermann ◽  
E J Gianatti ◽  
E J Hamilton ◽  
...  

2008 ◽  
Vol 93 (12) ◽  
pp. 4969-4973 ◽  
Author(s):  
Blerina Kola ◽  
Mirjam Christ-Crain ◽  
Francesca Lolli ◽  
Giorgio Arnaldi ◽  
Gilberta Giacchetti ◽  
...  

Objective: Features of the metabolic syndrome such as central obesity with insulin resistance and dyslipidemia are typical signs of Cushing’s syndrome and common side effects of prolonged glucocorticoid treatment. AMP-activated protein kinase (AMPK), a key regulatory enzyme of lipid and carbohydrate metabolism as well as appetite, is involved in the development of the deleterious metabolic effects of excess glucocorticoids, but no data are available in humans. In the current study, we demonstrate the effect of high glucocorticoid levels on AMPK activity of human adipose tissue samples from patients with Cushing’s syndrome. Methods: AMPK activity and mRNA expression of genes involved in lipid metabolism were assessed in visceral adipose tissue removed at abdominal surgery of 11 patients with Cushing’s syndrome, nine sex-, age-, and weight-matched patients with adrenal incidentalomas, and in visceral adipose tissue from four patients with non-endocrine-related abdominal surgery. Results: The patients with Cushing’s syndrome exhibited a 70% lower AMPK activity in visceral adipose tissue as compared with both incidentalomas and control patients (P = 0.007 and P < 0.001, respectively). Downstream targets of AMPK fatty acid synthase and phosphoenol-pyruvate carboxykinase were up-regulated in patients with Cushing’s syndrome. AMPK activity was inversely correlated with 0900 h serum cortisol and with urinary free cortisol. Conclusions: Our data suggest that glucocorticoids inhibit AMPK activity in adipose tissue, suggesting a novel mechanism to explain the deposition of visceral adipose tissue and the consequent central obesity observed in patients with iatrogenic or endogenous Cushing’s syndrome.


Obesity ◽  
2012 ◽  
Vol 20 (6) ◽  
pp. 1293-1300 ◽  
Author(s):  
Scott A. Lear ◽  
Arun Chockalingam ◽  
Simi Kohli ◽  
Chris G. Richardson ◽  
Karin H. Humphries

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Andreas Kammerlander ◽  
Asya Lyass ◽  
Taylor Mahoney ◽  
Joseph Massaro ◽  
Michelle T Long ◽  
...  

Background: The current clinical practice of defining obesity based on body mass index (BMI) does not capture differences in fat distribution between men and women. Visceral adipose tissue (VAT) as measured by computed tomography (CT), is an advanced measure of obesity that closely correlates with cardiometabolic risk independent of BMI. However, it remains unknown whether VAT adds additional prognostic significance over BMI in men or women. Methods: In participants of the Framingham Heart Study, we tested the associations of BMI and VAT with incident cardiometabolic events (diabetes, hypertension, low HDL, hypertriglyceridemia), and incident cardiovascular events and death. Mean follow-up was 12.7±2.1 years. Logistic and Cox-regression models were adjusted for age and smoking and adjusted odds and hazard ratios (adj. OR, adj. HR), are presented per 1-SD increase of each measure of body fat. Results: The study cohort comprised 3,482 participants (48.1% women, 50.8±10.3 years old). In men, VAT, as compared to BMI, had a similar strength of association with all cardiometabolic outcomes and incident cardiovascular disease (Figure). In women, however, VAT conferred a markedly greater association with incident cardiometabolic and cardiovascular disease compared to BMI (Figure). Conclusion and Relevance: BMI adequately captures VAT-associated cardiometabolic and cardiovascular risk in men but not in women. In women, abdominal CT-based VAT measures permit more precise assessment of obesity-associated cardiometabolic and cardiovascular risk.


Author(s):  
Guido Lastra ◽  
Camila Manrique

AbstractObesity is a leading risk factor for the development of type 2 diabetes mellitus (DM2) and cardiovascular disease (CVD), however the underlying mechanisms still remain to be fully uncovered. It is now well accepted that dysfunctional adipose tissue in conditions of obesity is a critical source of inflammation that impacts the cardiovascular system and contributes to CVD. Although traditionally visceral adipose tissue has been linked to increased CVD risk, there is mounting interest in the role that fat accumulation around the vasculature plays in the pathogenesis of vascular dysfunction. Perivascular adipose tissue (PVAT) is in intimate contact with large, medium and small diameter arterial beds in several tissues, and has been shown to control vascular function as well as remodeling. PVAT does not merely mirror visceral adipose tissue changes seen in obesity, but has unique features that impact vascular biology. In lean individuals PVAT exerts vasodilatory and anti-inflammatory functions, however obesity results in PVAT inflammation, characterized by imbalance between pro- and anti-inflammatory cells as wells as adipokines. PVAT inflammation promotes insulin resistance in the vasculature, thus resulting in impaired insulin-mediated vasodilatory responses and vascular remodeling. In this review we address current knowledge about the mechanisms that link PVAT inflammation to insulin resistance and vascular dysfunction. Indeed, PVAT emerges as a novel type of adipose tissue that participates in the pathogenesis of CVD, independently to a large extent to visceral adipose tissue.


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