The University of Southampton
University of Southampton Institutional Repository

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.

Full text not available from this repository.

More information

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

Catalogue record

Date deposited: 20 Apr 2010 09:07
Last modified: 17 Dec 2019 01:52

Export record

Altmetrics

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of http://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×