This review highlights the central role of inflammation and oxidative stress in the pathogenesis of metabolic syndrome and its associated cardiovascular risks.
Supports mechanistic research on inflammation in metabolic syndrome; leaves open targeted therapies pending interventional trials.
The metabolic consequences of obesity have made this highly prevalent condition one of the most common risk factors for type 2 diabetes, hypertension and atherosclerosis. Simultaneous occurrence of these conditions can be explained through the manifestations of metabolic syndrome [MetS]. Clinical indication of MetS is characterized by a clustering of risk factors for complex chronic diseases which all feature metabolic deterioration as a common component. Diagnosis of MetS can be made if a patient exhibits three of the identified risk factors, some of which include: elevated waist circumference, elevated triglycerides, low high density lipoprotein levels, hypertension and elevated blood glucose. The progression from obesity to MetS involves an alteration in body metabolism mediated by cytokines- signalling molecules that coordinate the inflammatory response. Increased visceral adipose tissue contributes to augmented secretion of pro-inflammatory cytokines which can activate several transcription factors, including NF-κB, which promote these inflammatory conditions and lead to increased oxidative stress. Exacerbation of the condition then ensues as oxidative stress results in oxidized low density lipoprotein, dyslipidemia, insulin resistance, hypertension and atherogenesis. This review will not only focus on the role of inflammation in the manifestations of MetS, but also outlines some lifestyle and nutritional treatments that can be used to treat the condition and reduce the risk of chronic disease.
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Cristina Cuda (2008) studied this question.
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