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Table of Contents
Vol. 113, No. 1-4, 2006
Issue release date: March 2006
Section title: Human Disease
Cytogenet Genome Res 113:279–291 (2006)
(DOI:10.1159/000090843)

Regulation of growth and metabolism by imprinted genes

Smith F.M. · Garfield A.S. · Ward A.
Centre for Regenerative Medicine and Developmental Biology Programme, University of Bath, Department of Biology and Biochemistry, Bath (UK)

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Article / Publication Details

First-Page Preview
Abstract of Human Disease

Published online: March 30, 2006
Issue release date: March 2006

Number of Print Pages: 13
Number of Figures: 1
Number of Tables: 3

ISSN: 1424-8581 (Print)
eISSN: 1424-859X (Online)

For additional information: http://www.karger.com/CGR

Abstract

A small sub-set of mammalian genes are subject to regulation by genomic imprinting such that only one parental allele is active in at least some sites of expression. Imprinted genes have diverse functions, notably including the regulation of growth. Much attention has been devoted to the insulin-like growth factor signalling pathway that has a major influence on fetal size and contains two components encoded by the oppositely imprinted genes, Igf2 (a growth promoting factor expressed from the paternal allele) and Igf2r (a growth inhibitory factor expressed from the maternal allele). These genes fit the parent-offspring conflict hypothesis for the evolution of genomic imprinting. Accumulated evidence indicates that at least one other fetal growth pathway exists that has also fallen under the influence of imprinting. It is clear that not all components of growth regulatory pathways are encoded by imprinted genes and instead it may be that within a pathway the influence of a single gene by each of the parental genomes may be sufficient for parent-offspring conflict to be enacted. A number of imprinted genes have been found to influence energy homeostasis and some, including Igf2 and Grb10, may coordinate growth with glucose-regulated metabolism. Since perturbation of fetal growth can be correlated with metabolic disorders in adulthood these imprinted genes are considered as candidates for involvement in this phenomenon of fetal programming.

© 2006 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Human Disease

Published online: March 30, 2006
Issue release date: March 2006

Number of Print Pages: 13
Number of Figures: 1
Number of Tables: 3

ISSN: 1424-8581 (Print)
eISSN: 1424-859X (Online)

For additional information: http://www.karger.com/CGR


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