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Updated: May 11, 2026
Assessment of Human Adipose Tissue Microvascular Function Using Videomicroscopy
Published on: September 29, 2017
Cyclooxygenase inhibition improves endothelial vasomotor dysfunction of visceral adipose arterioles in human obesity
Melissa G Farb1, Stephanie Tiwari, Shakun Karki
1Department of Medicine and Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Massachusetts, USA.
Objective:
The purpose of this study was to determine whether cyclooxygenase inhibition improves vascular dysfunction of adipose microvessels from obese humans.
Design And Methods:
In 20 obese subjects (age 37 ± 12 years, BMI 47 ± 8 kg/m²), subcutaneous and visceral fat were collected during bariatric surgery and characterized for adipose depot-specific gene expression, endothelial cell phenotype, and microvascular function. Vasomotor function was assessed in response to endothelium-dependent agonists using videomicroscopy of small arterioles from fat.
Results:
Arterioles from visceral fat exhibited impaired endothelium-dependent, acetylcholine-mediated vasodilation, compared to the subcutaneous depot (P < 0.001). Expression of mRNA transcripts relevant to the cyclooxygenase pathway was upregulated in visceral compared to subcutaneous fat. Pharmacological inhibition of cyclooxygenase with indomethacin improved endothelium-dependent vasodilator function of arterioles from visceral fat by twofold (P = 0.01), whereas indomethacin had no effect in the subcutaneous depot. Indomethacin increased activation via serine-1177 phosphorylation of endothelial nitric oxide synthase in response to acetylcholine in endothelial cells from visceral fat. Inhibition of endothelial nitric oxide synthase with N(ω)-nitro-L-arginine methyl ester abrogated the effects of cyclooxygenase-inhibition suggesting that vascular actions of indomethacin were related to increased nitric oxide bioavailability.
Conclusions:
Our findings suggest that cyclooxygenase-mediated vasoconstrictor prostanoids partly contribute to endothelial dysfunction of visceral adipose arterioles in human obesity.
Insights
Cyclooxygenase inhibition improved blood vessel function in visceral fat of obese individuals. This suggests that blocking cyclooxygenase may help treat endothelial dysfunction in obesity.
Area of Science:
- Vascular Biology
- Obesity Research
- Pharmacology
Background:
- Obesity is linked to endothelial dysfunction and impaired microvascular function.
- Adipose tissue microvessels show depot-specific differences in function and gene expression.
Purpose of the Study:
- To investigate the effect of cyclooxygenase inhibition on vascular dysfunction in adipose microvessels from obese humans.
- To determine if targeting cyclooxygenase can improve endothelial function in visceral fat.
Main Methods:
- Collected subcutaneous and visceral fat from 20 obese subjects undergoing bariatric surgery.
- Assessed microvascular function using videomicroscopy of small arterioles.
- Analyzed gene expression and endothelial cell phenotype.
- Administered cyclooxygenase inhibitor (indomethacin) and nitric oxide synthase inhibitor (N(ω)-nitro-L-arginine methyl ester).
Main Results:
- Visceral fat arterioles showed impaired vasodilation compared to subcutaneous fat.
- Cyclooxygenase pathway transcripts were upregulated in visceral fat.
- Indomethacin significantly improved vasodilation in visceral fat arterioles by twofold.
- Indomethacin increased endothelial nitric oxide synthase activation, and its effects were abolished by nitric oxide synthase inhibition.
Conclusions:
- Cyclooxygenase-mediated vasoconstrictor prostanoids contribute to endothelial dysfunction in visceral adipose arterioles in human obesity.
- Targeting cyclooxygenase may be a therapeutic strategy to improve vascular function in obesity-related endothelial dysfunction.
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