Metabolic
 Prof Harold David McIntyre
Metabolic "programming" in pregnancy
Placental and adipose tissue inflammatory markers and insulin resistance in normal and obese pregnancy
Background
It is recognised that the extremes of size and adiposity at birth are associated with increased rates of coronary heart disease, hypertension and type 2 diabetes mellitus (T2DM) in later adult life. Unfortunately little is known about the precise molecular mechanisms involved in (dys)regulation of fetal growth. Both small and large for gestational age babies suffer an increased risk of later cardiovascular disease. (1)
The consequences of interventions to regulate fetal growth are likely to have lifelong health benefits for the offspring, in particular a reduction in the risk of coronary heart disease and T2DM.
Aim
Both placental and adipose tissue inflammation may serve to create an abnormal metabolic state in mother and baby, favouring fat deposition and future adiposity and forming part of the mechanism of metabolic “programming” in pregnancy. The aim of the current application is to examine the relationships between insulin resistance and serum / placental / adipose tissue cellular and cytokine / hormonal profiles in normal and obese pregnant women.
Research questions / hypotheses
- Obese pregnant women will show higher levels of inflammatory cytokines in serum, placenta and adipose tissue.
- Obese pregnant women will have denser populations of placental and adipose tissue macrophages, with different immunologic phenotypes
- Inflammatory markers (tissue and serum) will correlate with in vivo measures of insulin sensitivity.
- Levels of inflammatory cytokines and adipocytokines will vary between omental and subcutaneous adipose tissue
- The relationships between maternal and fetal adipocytokines will be examined
|
