Functional Relationship between Arterial Tissue and Perivascular Adipose Tissue in Metabolic Syndrome

Abstract

Metabolic syndrome is a complex of disorders that includes visceral obesity, insulin resistance, hypertension, and dyslipidemia. It is characterized by an increased risk for serious cardiovascular events. Adipocytes are now recognized to contribute to the development of cardiovascular complications in metabolic syndrome via the release of several bioactive substances (adipocytokines). Obesity induces an increase in the volume of perivascular adipose tissue (PVAT), which is located outside the blood vessels. In recent years, PVAT has been reported to produce/release vasoactive adipocytokines. Thus, PVAT can modulate vasomotor function by releasing vasorelaxing/vasocontracting factors, resulting in the development of cardiovascular disease due to metabolic syndrome. By using animal models (SHR/ NDmcr-cp rats, SHRSP.Z-Lepr fa /IzmDmcr rats, and B6.BKS (D)-Lepr fa /J mice), we have demonstrated that chronic oxidative-nitrative stress is closely linked to the development of vascular dysfunction in response to nitric oxide (NO) in resistant arteries with increasing age/exposure to metabolic abnormalities. Further, our recentˆndings have led us to believe that PVAT helps in the regulation of vasodilation to compensate for the impaired vasodilation observed in pathophysiological conditions in the mesenteric arteries of SHRSP.Z-Lepr fa /IzmDmcr rats. However, a breakdown of the compensatory system occurs with long-term exposure to metabolic abnormalities. We propose the concept of the functional regulation of vascular tissue by PVAT in metabolic syndrome.

Perivascular Adipose Tissue-Enhanced Vasodilation in Metabolic Syndrome Rats by Apelin and N-Acetyl–l-Cysteine-Sensitive Factor(s)

“…MetS is a chronic condition which worsens with time and thus, requires long-term strategies for clinical treatment. Our previous studies show that mesenteric PVAT has compensatory effects to maintain vascular tonus under the condition of impaired NO-mediated relaxations in SHRSP.ZF (at 20 wks), i.e., PVAT enhances vasodilation in response to either endothelium-derived NO induced by acetylcholine or exogenous NO derived from sodium nitroprusside in mesenteric artery of SHRSP.ZF [4,30,31]. However, the compensatory function of PVAT was impaired at a later stage of MetS (at 30 wks).…”

Body Mass Index Is Associated With Microvascular Endothelial Dysfunction in Patients With Treated Metabolic Risk Factors and Suspected Coronary Artery Disease

“…Only recently perivascular adipose tissue, which is increased in obesity, has been shown to be of influence in microvascular function. In addition to the lamina intima, media, and adventitia, it is described as the fourth vessel wall layer, and this tissue has an important role in vasomotor regulation by excreting vasoactive adipocytokines . Under normal circumstances, perivascular adipose tissue functions in a paracrine fashion, directly reducing smooth muscle tone and enhancing insulin‐dependent vasodilatation.…”

Alzheimer's disease and metabolic syndrome: A link from oxidative stress and inflammation to neurodegeneration

“…On the other hand, metabolic syndrome (MetS) is defined as the concurrence of obesity‐associated cardiovascular risk factors including abdominal obesity, impaired glucose tolerance, hypertriglyceridemia, decreased High density lipoprotein (HDL) cholesterol, and/or hypertension (Tune, Goodwill, Sassoon, & Mather, ). It is a widely spread condition that increases vascular risk, due to the impact of its components on oxidative stress, chronic inflammation, and metabolic dysregulation, which ultimately lead in most scenarios to adverse endocrine and microvascular outcomes (Kagota, Iwata, Maruyama, Wakuda, & Shinozuka, ; Rani, Deep, Singh, Palle, & Yadav, ).…”