title: 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 recent findings 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.
authors.affiliation: Department of Pharmacology II, School of Pharmacy and Pharmaceutical Sciences, Mukogawa Women's University.
authors.forename: Satomi
authors.initials: S
authors.lastname: Kagota
authors.forename: Saki
authors.initials: S
authors.lastname: Iwata
authors.forename: Kana
authors.initials: K
authors.lastname: Maruyama
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Wakuda
authors.forename: Kazumasa
authors.initials: K
authors.lastname: Shinozuka
mesh_terms: D017667:Adipocytes / Q000378:metabolism / Q000502:physiology; D054392:Adipokines / Q000378:metabolism / Q000502:physiology; D000273:Adipose Tissue / Q000378:metabolism / Q000473:pathology / Q000502:physiology*; D000818:Animals; D001158:Arteries / Q000502:physiology* / Q000503:physiopathology*; D002318:Cardiovascular Diseases / Q000209:etiology*; D004195:Disease Models, Animal; D006801:Humans; D024821:Metabolic Syndrome / Q000150:complications* / Q000503:physiopathology*; D051379:Mice; D009569:Nitric Oxide; D009765:Obesity / Q000473:pathology; D018384:Oxidative Stress / Q000502:physiology; D051381:Rats; D012306:Risk; D014662:Vasoconstrictor Agents / Q000378:metabolism; D014664:Vasodilation; D014665:Vasodilator Agents / Q000378:metabolism
chemical_list: D054392:Adipokines; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009569:Nitric Oxide