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The developmental origins, mechanisms, and implications of metabolic syndrome

The developmental origins, mechanisms, and implications of metabolic syndrome
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 prevalence of MetS is rapidly increasing worldwide, largely as a consequence of the ongoing obesity epidemic. Environmental factors during periods 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 mechanisms by which nutritional insults during a period of developmental plasticity result in a MetS phenotype are now beginning to receive considerable scientific interest. This review focuses on recent data regarding these mechanisms, in particular the 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 interventions, with a favorable impact on the global incidence of cardiovascular disease and type 2 diabetes in the future.
0022-3166
648-652
Bruce, K.D.
1ded890b-addf-45bd-ba59-dbaedaeee931
Hanson, Mark A.
1952fad1-abc7-4284-a0bc-a7eb31f70a3f
Bruce, K.D.
1ded890b-addf-45bd-ba59-dbaedaeee931
Hanson, Mark A.
1952fad1-abc7-4284-a0bc-a7eb31f70a3f

Bruce, K.D. and Hanson, Mark A. (2010) The developmental origins, mechanisms, and implications of metabolic syndrome. Journal of Nutrition, 140 (3), 648-652. (doi:10.3945/jn.109.111179).

Record type: Article

Abstract

Metabolic syndrome (MetS) represents a combination of cardio-metabolic risk determinants, including central obesity, insulin resistance, glucose intolerance, dyslipidemia, hypertension, hyperinsulinemia, and microalbuminuria. The prevalence of MetS is rapidly increasing worldwide, largely as a consequence of the ongoing obesity epidemic. Environmental factors during periods 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 mechanisms by which nutritional insults during a period of developmental plasticity result in a MetS phenotype are now beginning to receive considerable scientific interest. This review focuses on recent data regarding these mechanisms, in particular the 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 interventions, with a favorable impact on the global incidence of cardiovascular disease and type 2 diabetes in the future.

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e-pub ahead of print date: 27 January 2010
Published date: March 2010

Identifiers

Local EPrints ID: 145775
URI: http://eprints.soton.ac.uk/id/eprint/145775
ISSN: 0022-3166
PURE UUID: ba2c0e86-7e58-4a91-a4d9-119675922791
ORCID for Mark A. Hanson: ORCID iD orcid.org/0000-0002-6907-613X

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Date deposited: 20 Apr 2010 09:07
Last modified: 14 Mar 2024 02:44

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Contributors

Author: K.D. Bruce
Author: Mark A. Hanson ORCID iD

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