Epigenetic regulation of transcription: a mechanism for inducing variations in phenotype (fetal programming) by differences in nutrition during early life?

被引:238
作者
Burdge, Graham C. [1 ]
Hanson, Mark A. [1 ]
Slater-Jefferies, Jo L. [1 ]
Lillycrop, Karen A. [1 ]
机构
[1] Univ Southampton, DOHaD Res Div, Southampton SO16 7PX, Hants, England
关键词
epigenetic regulation; fetal programming; metabolic disease; DNA methylation; DNA methyltransferase;
D O I
10.1017/S0007114507682920
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
There is considerable evidence for the induction of different phenotypes by variations in the early life environment, including nutrition, which in man is associated with a graded risk of metabolic disease; fetal programming. It is likely that the induction of persistent changes to tissue structure and function by differences in the early life environment involves life-long alterations to the regulation of gene transcription. This view is supported by both studies of human subjects and animal models. The mechanism which underlies such changes to gene expression is now beginning to be understood. In the present review we discuss the role of changes in the epigenetic regulation of transcription, specifically DNA methylation and covalent modification of histones, in the induction of an altered phenotype by nutritional constraint in early life. The demonstration of altered epigenetic regulation of genes in phenotype induction suggests the possibility of interventions to modify long-term disease risk associated with unbalanced nutrition in early life.
引用
收藏
页码:1036 / 1046
页数:11
相关论文
共 92 条
[1]  
[Anonymous], 2005, The fetal matrix: evolution, development and disease
[2]   Experimental models of developmental programming: consequences of exposure to an energy rich diet during development [J].
Armitage, JA ;
Taylor, PD ;
Poston, L .
JOURNAL OF PHYSIOLOGY-LONDON, 2005, 565 (01) :3-8
[3]   Developmental programming of the metabolic syndrome by maternal nutritional imbalance: how strong is the evidence from experimental models in mammals? [J].
Armitage, JA ;
Khan, IY ;
Taylor, PD ;
Nathanielsz, PW ;
Poston, L .
JOURNAL OF PHYSIOLOGY-LONDON, 2004, 561 (02) :355-377
[4]   Developmental plasticity and human health [J].
Bateson, P ;
Barker, D ;
Clutton-Brock, T ;
Deb, D ;
D'Udine, B ;
Foley, RA ;
Gluckman, P ;
Godfrey, K ;
Kirkwood, T ;
Lahr, MM ;
McNamara, J ;
Metcalfe, NB ;
Monaghan, P ;
Spencer, HG ;
Sultan, SE .
NATURE, 2004, 430 (6998) :419-421
[5]   SEQUENTIAL-CHANGES IN DNA METHYLATION PATTERNS OF THE RAT PHOSPHOENOLPYRUVATE CARBOXYKINASE GENE DURING DEVELOPMENT [J].
BENVENISTY, N ;
MENCHER, D ;
MEYUHAS, O ;
RAZIN, A ;
RESHEF, L .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1985, 82 (02) :267-271
[6]   Glucose metabolism is altered in the adequately-nourished grand-offspring (F3 generation) of rats malnourished during gestation and perinatal life [J].
Benyshek, DC ;
Johnston, CS ;
Martin, JF .
DIABETOLOGIA, 2006, 49 (05) :1117-1119
[7]   The maternal diet during pregnancy programs altered expression of the glucocorticoid receptor and type 2 11β-hydroxysteroid dehydrogenase:: Potential molecular mechanisms underlying the programming of hypertension in utero [J].
Bertram, C ;
Trowern, AR ;
Copin, N ;
Jackson, AA ;
Whorwood, CB .
ENDOCRINOLOGY, 2001, 142 (07) :2841-2853
[8]   Animal models and programming of the metabolic syndrome [J].
Bertram, CE ;
Hanson, MA .
BRITISH MEDICAL BULLETIN, 2001, 60 :103-121
[9]   Dnmt1 overexpression causes genomic hypermethylation, loss of imprinting, and embryonic lethality [J].
Biniszkiewicz, D ;
Gribnau, J ;
Ramsahoye, B ;
Gaudet, F ;
Eggan, K ;
Humpherys, D ;
Mastrangelo, MA ;
Jun, Z ;
Walter, J ;
Jaenisch, R .
MOLECULAR AND CELLULAR BIOLOGY, 2002, 22 (07) :2124-2135
[10]   DNA methylation patterns and epigenetic memory [J].
Bird, A .
GENES & DEVELOPMENT, 2002, 16 (01) :6-21