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Comparative Study
. 2012 Feb;32(2):467-73.
doi: 10.1161/ATVBAHA.111.235846. Epub 2011 Nov 17.

Arteriolar function in visceral adipose tissue is impaired in human obesity

Melissa G Farb  1 , Lisa Ganley-Leal, Melanie Mott, Yanmei Liang, Bahadir Ercan, Michael E Widlansky, Sherman J Bigornia, Antonino J Fiscale, Caroline M Apovian, Brian Carmine, Donald T Hess, Joseph A Vita, Noyan Gokce
Affiliations
Comparative Study

Arteriolar function in visceral adipose tissue is impaired in human obesity

Melissa G Farb et al. Arterioscler Thromb Vasc Biol. 2012 Feb.

Abstract

Objective: The purpose of this study was to characterize the relationship between adipose tissue phenotype and depot-specific microvascular function in fat.

Methods and results: In 30 obese subjects (age 42±11 years, body mass index 46±11 kg/m(2)) undergoing bariatric surgery, we intraoperatively collected visceral and subcutaneous adipose tissue and characterized depot-specific adipose phenotypes. We assessed vasomotor function of the adipose microvasculature using videomicroscopy of small arterioles (75-250 μm) isolated from different fat compartments. Endothelium-dependent, acetylcholine-mediated vasodilation was severely impaired in visceral arterioles, compared to the subcutaneous depot (P<0.001 by ANOVA). Nonendothelium dependent responses to papaverine and nitroprusside were similar. Endothelial nitric oxide synthase inhibition with N(ω)-nitro-l-arginine methyl ester reduced subcutaneous vasodilation but had no effect on severely blunted visceral arteriolar responses. Visceral fat exhibited greater expression of proinflammatory, oxidative stress-related, hypoxia-induced, and proangiogenic genes; increased activated macrophage populations; and had a higher capacity for cytokine production ex vivo.

Conclusions: Our findings provide clinical evidence that the visceral microenvironment may be intrinsically toxic to arterial health providing a potential mechanism by which visceral adiposity burden is linked to atherosclerotic vascular disease. Our findings also support the evolving concept that both adipose tissue quality and quantity may play significant roles in shaping cardiovascular phenotypes in human obesity.

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Figures

Figure 1
Figure 1. Adipose tissues arteriolar responses
Endothelium-dependent, Ach-mediated vasodilation was severely impaired in visceral compared to sc adipose tissue arterioles (p<0.001 by ANOVA), while responses to papaverine were similar (n=40). Data presented as mean ± SEM.
Figure 2
Figure 2. Effect of L-NAME on adipose vasomotor responses
L-NAME (10−4 M) reduced vasodilator responses in subcutaneous microvessels indicating partial dependence on nitric oxide bioaction (n=6, P=0.005 by ANOVA). (B) In contrast, L-NAME had no effect on severely blunted visceral arteriolar responses (n=6, P=0.36 by ANOVA). Data are presented as mean ± SEM.
Figure 3
Figure 3. Depot-specific macrophage polarization in adipose tissue
Adipose flow cytometry identified higher populations of (A) TLR4+ M1 polarized macrophages in visceral vs. sc adipose tissue. Similarly, macrophages expressing markers traditionally associated with M2 phenotypes (B) CD209 and (C) CD206 were also significantly higher in visceral fat. ***p<0.001; **p<0.01 compared to subcutaneous depot. Data presented as mean ± SEM.
Figure 4
Figure 4. Cytokine production in cultured adipose tissue leukocytes
Basal IL-6 (A) and IL-8 (B) secretion was higher in leukocytes isolated from visceral compared to sc adipose tissue. LPS stimulation significantly increased IL-6 production. ***p<0.001; **p<0.01; *p<0.05 versus subcutaneous depot. Data presented as mean ± SEM.
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