The developmental origins, mechanisms, and implications of metabolic syndrome

Metabolic syndrome (MetS) represents a combination of cardio-metabolic risk determinants, including central obesity, insulin resistance, glucose intolerance, dyslipidemia, hypertension, hyperinsulinemia, and microalbuminuria. The prevalance of MetS is rapidly increasing worldwide, largely as a consequence of the ongoing obesity epidemic. Environmental factors during period early in development have been shown to influence the susceptibility to develop disease in later life. In particular, there is a wealth of evidence from both epidemiological and animal studies for greater incidence of features of MetS as a result of unbalanced maternal nutrition. The mechanism by which nutritional insults during a period of development plasticity result in MetS phenotype are now beginning to receive considerable scientific interest. This review focuses on recent data regarding these mechanisms, in particular epigenetic and transcriptional regulation of key metabolic genes in response to nutritional stimuli that mediate persistent changes and an adult MetS phenotype. A continued and greater understanding of these mechanisms will eventually allow specific intervention, with a favorable impact on the global incidence of cardiovascular disease and type 2 diabetes in the future.