CONTEXT: Endothelium guarantees vascular homeostasis by the opposite action of 
substances by vasodilating/antithrombogenic and vasoconstricting/prothrombotic 
activities. Obesity is characterized by endothelial dysfunction associated with 
a condition of vascular low-grade inflammation.
EVIDENCE ACQUISITION: Analysis of available basic or clinical papers published 
in peer-reviewed international journals on microcirculation and obesity.
EVIDENCE SYNTHESIS: Vascular low-grade inflammation, which characterizes 
obesity, is secondary to abnormal production of proinflammatory cytokines, 
including TNF-α. TNF-α, generated either in small vessels or within the 
perivascular adipose tissue (PVAT) of patients with obesity, stimulates reactive 
oxygen species generation, mainly through NAD(P)H oxidase activation, which in 
turn reduces nitric oxide (NO) availability. These aspects are highlighted by 
the insulin resistance status and macronutrient intake that characterize the 
obesity condition. Oxidant excess has also been proposed as a mechanism whereby 
TNF-α interferes with the endothelin-1/NO system at the level of small vessels 
from patients with obesity.
CONCLUSIONS: In obesity, microvasculature from visceral fat is an important 
source of low-grade inflammation and oxidative stress that, together with the 
PVAT, directly contribute to vascular changes, favoring the development and 
acceleration of the vascular atherothrombotic process in this clinical 
condition.