Maternal and Fetal Physiology

This group focuses its research on the mechanisms by which maternal diet, body
composition, metabolism and endocrine status influence the development of the fetus
and neonate, programming its risk of chronic disease in later life. Research involves
an integration of a range of experimental approaches, from genomics to systems
physiology and utilises animal models and studies of human pregnancy.

We have established that maternal diet and body composition can influence placental
growth and have long-term effects on the offspring. Low maternal birthweight has
been found to impair a womans subsequent capacity to supply nutrients to her fetus,
resulting in a reduced growth trajectory in late gestation and thinness of the offspring
at birth. Using the rat model, studies have shown that low protein intakes during
pregnancy lead to persistent changes in the HPA axis, at both the pituitary and
adrenal levels, in responses to glucocorticoid-sensitive tissues and also shows
effects on the preimplantation embryo. Fetal mechanisms are explored in the sheep
model, in which the group have also shown that dietary restriction in early gestation
produces re-setting of cardiovascular and endocrine control in the late gestation fetus
and postnatal lamb.


Scientific enquiries: Dr L Green Email: L.R.Green@soton.ac.uk

Visit our web page:
http://www.som.soton.ac.uk/research/foad/maternal_fetal_physiology.asp


Professor Mark Hanson
Email: M.Hanson@soton.ac.uk
http://www.som.soton.ac.uk/research/foad/hanson.asp

This area of work at Southampton has been established by the creation of new
research facilities within the FOAD Centre and the Biomedical Research Facilities at
SGH. The current programme includes detailed studies of the development and
functional control of the cardiovascular, endocrine and respiratory systems, and of
the brain and behaviour. Several species and methods of investigating the effects of
developmental perturbation are used.

Currently the main issues being addressed in relation to the FOAD hypothesis are:

What are the mechanisms by which moderate undernutrition in early
pregnancy alters placental growth and function?

How does moderate undernutrition in early pregnancy affect cardiovascular
development and function, especially blood pressure and its control?

What produces the changes which we have found in animals in fetal HPA axis
sensitivity following moderate undernutrition in early pregnancy? The
molecular aspects of this study are conducted in collaboration with Dr.
Stephen Matthews (Toronto).

What role do changes in small artery responses play in the programming of elevated
blood pressure development? Of particular interest are the effects of vascular
endothelial cell function. This area of work encompasses an extensive collaboration
with Prof. Lucilla Poston (GKT London) and is funded by the British Heart
Foundation.


Professor Iain T. Cameron
Email: itc@soton.ac.uk
http://www.som.soton.ac.uk/research/foad/cameron.asp

The focus of research is within the following areas:

investigations into the maternal environment in early pregnancy (linking
closely with Professor Tom Flemings team at the Boldrewood campus),
building upon previous studies of paracrine mechanisms in the uterus.

determination of whether nutritional effects on the preimplantation embryo are
mediated via changes in the paracrine function of the uterus and Fallopian
tube.

exploration of the pathophysiology of intrauterine growth restriction by
measuring placental gene expression and determining endothelial cell
function in normal and growth-restricted fetuses.


Dr Lucy Green
Email: lgreen@soton.ac.uk
https://www.som.soton.ac.uk/research/foad/green.asp

By combining whole systems physiology, conventional endocrinology and molecular
biology techniques an integrative approach is used in the fetus and neonate to study:

The effect of maternal diet on fetal and postnatal cardiovascular development
and growth

Programming of reflex neuronal (e.g. peripheral chemoreceptors) and hormonal
mechanisms (e.g. renin angiotensin system and hypothalamo-pituitary-adrenal
axis) of cardiovascular control

Mechanisms underlying fetal growth, including the insulin-like growth factor
system.


Dr Keith Godfrey
Email: kmg@mrc.soton.ac.uk
http://www.som.soton.ac.uk/research/foad/godfrey.asp


The aims of this programme of work within the MRC Environmental Epidemiology
Unit are

to understand the maternal regulation of fetal growth and development

to define how maternal diet and body composition can be optimised to improve
the health of the offspring in later childhood and adult life.

Ongoing studies within the Southampton Womens Survey seek to

characterise the effects of a womans diet and body composition before and
during pregnancy on fetal growth, and address intergenerational effects of a
womans own growth in utero on the growth of her fetus

examine the hypothesis that the long-term effects of impaired fetal development
are consequences of fetal developmental adaptations that occur when the
materno-placental supply of nutrients fails to match fetal demand

define how alterations in placental function and fetal cardiovascular adaptations
may programme cardiovascular and metabolic disease in later life.


Mr Timothy Wheeler
E-mail: tw2@soton.ac.uk
http://www.som.soton.ac.uk/research/foad/Wheeler.asp

The focus of research is within the following areas:

the effects of maternal nutrition on the vascular function of her offspring with
specific attention to modifications of the nitric oxide pathway.

the contribution of the maternal cardiovascular system to fetal growth with
particular reference to prenatal vascular function.


Control of cellular function in reproductive tissues

Dr Malcolm C Richardson
Email: M.C.Richardson@soton.ac.uk
http://www.som.soton.ac.uk/research/tissue/members/mcr2.htm

Students are invited to join research teams in the following areas:

extracellular matrix control through metalloproteinases in ovarian granulosa cells

insulin sensitivity of granulosa cells in relation to polycystic ovary disease

role of insulin-like growth factor binding proteins in oviduct function