This review highlights the role of inflammatory mediators in the progression of metabolic syndrome, suggesting potential therapeutic targets to alter disease progression.
Potential targets in metabolic syndrome warrant trials; leaves open whether modulating these mediators improves outcomes.
The metabolic syndrome is often associated with type 2 diabetes mellitus, dyslipidemia, atherosclerosis, hypertension, steatosis of the liver and other organs, as well as hypertension, type 2 diabetes mellitus, and atherosclerosis. Recent studies have implicated a number of inflammatory mediators including cytokines, adipokines and eicosanoids in the inflammatory responses that accompany the metabolic syndrome. Measurements of the circulating levels of the inflammatory molecules that accompany this syndrome might provide leads to therapeutic approaches to modulate the inflammatory responses and thereby alter disease progression. In this review, we summarize recent studies on classical and newer inflammatory mediators in the pathogenesis of the metabolic syndrome in humans and experimental models.
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Ma et al. (2012) studied this question.
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