Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 88-94 |
| Number of pages | 7 |
| Journal | Medical hypotheses |
| Volume | 78 |
| Issue number | 1 |
| Early online date | 1 Nov 2011 |
| DOIs | |
| Publication status | Published - Jan 2012 |
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A common cause for a common phenotype : the gatekeeper hypothesis in fetal programming. / McMullen, S; Langley-Evans, S C; Gambling, L; Lang, C; Swali, A; McArdle, H J.
In: Medical hypotheses, Vol. 78, No. 1, 01.2012, p. 88-94.Research output: Contribution to journal › Article
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TY - JOUR
T1 - A common cause for a common phenotype
T2 - the gatekeeper hypothesis in fetal programming
AU - McMullen, S
AU - Langley-Evans, S C
AU - Gambling, L
AU - Lang, C
AU - Swali, A
AU - McArdle, H J
N1 - Copyright © 2011 Elsevier Ltd. All rights reserved.
PY - 2012/1
Y1 - 2012/1
N2 - Sub-optimal nutrition during pregnancy has been shown to have long-term effects on the health of offspring in both humans and animals. The most common outcomes of such programming are hypertension, obesity, dyslipidaemia and insulin resistance. This spectrum of disorders, collectively known as metabolic syndrome, appears to be the consequence of nutritional insult during early development, irrespective of the nutritional stress experienced. For example, diets low in protein diet, high in fat, or deficient in iron are all associated with programming of cardiovascular and metabolic disorders when fed during rat pregnancy. In this paper, we hypothesise that the nutritional stresses act on genes or gene pathways common to all of the insults. We have termed these genes and/or gene pathways the "gatekeepers" and hence developed the "gatekeeper hypothesis". In this paper, we examine the background to the hypothesis and postulate some possible mechanisms or pathways that may constitute programming gatekeepers.
AB - Sub-optimal nutrition during pregnancy has been shown to have long-term effects on the health of offspring in both humans and animals. The most common outcomes of such programming are hypertension, obesity, dyslipidaemia and insulin resistance. This spectrum of disorders, collectively known as metabolic syndrome, appears to be the consequence of nutritional insult during early development, irrespective of the nutritional stress experienced. For example, diets low in protein diet, high in fat, or deficient in iron are all associated with programming of cardiovascular and metabolic disorders when fed during rat pregnancy. In this paper, we hypothesise that the nutritional stresses act on genes or gene pathways common to all of the insults. We have termed these genes and/or gene pathways the "gatekeepers" and hence developed the "gatekeeper hypothesis". In this paper, we examine the background to the hypothesis and postulate some possible mechanisms or pathways that may constitute programming gatekeepers.
U2 - 10.1016/j.mehy.2011.09.047
DO - 10.1016/j.mehy.2011.09.047
M3 - Article
VL - 78
SP - 88
EP - 94
JO - Medical hypotheses
JF - Medical hypotheses
SN - 1532-2777
IS - 1
ER -