کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3002868 | 1180752 | 2007 | 8 صفحه PDF | دانلود رایگان |

AimThe prevalence of metabolic syndrome has increased dramatically in recent years, and the cluster of metabolic abnormalities it encompasses results in increased cardiovascular morbidity and mortality. The role of abdominal (visceral) obesity and the underlying molecular and cellular mechanisms central to this association have been the subject of intensive research in recent times. The aim of this review is to correlate data in this area, highlighting the central role of excess visceral fat and its secreted adipokines, and to review existing and emerging therapies.Data synthesisData were generated from a search of the PubMed database using the terms ‘abdominal obesity’, ‘metabolic syndrome’, ‘insulin resistance’, ‘adipokines’, ‘interleukin-6 (IL-6)’, ‘adiponectin’, ‘tumour necrosis factor-alpha (TNF-α)’ and ‘cardiovascular disease’.ConclusionMetabolic syndrome is associated with a pro-inflammatory state, and the role of visceral obesity is thought to be central to this. Visceral obesity leads to alteration of the normal physiological balance of adipokines, insulin resistance, endothelial dysfunction and a pro-atherogenic state. In association with this, the presence of conventional cardiovascular risk factors such as hypertension, dyslipidaemia and smoking results in a significantly elevated cardiovascular and metabolic (cardiometabolic) risk. Better understanding of the molecular mechanisms central to this association has led to the development of potential therapeutic agents.
Journal: Nutrition, Metabolism and Cardiovascular Diseases - Volume 17, Issue 4, May 2007, Pages 319–326