Obesity and it's consequences are emerging as a prime threat to health in the western world. During the last 20 years the prevalence of obesity has increased in all age groups, including children. This has led the search for etiological clues.
Several st udies have shown an association between low birth weight and adiposity in childhood and in adulthood. The mechanisms causing this are mostly unknown; however, the most intriguing is prenatal programming. Prenatal programming is a process, where a stimulus at a given time in fetal life can lead to lasting changes on the offspring. Exposures such as changes in maternal nutrition, hormonal status and fetal blood flow have been shown to lead to lasting changes in offspring in animal models.
The biochemical and endocrine pathways involved in prenatal programming are still unclear. One hypothesis suggests that one mechanism might be that the fetus is exposed to increased concentrations of stress hormone. Several animal models have suggested that exposure to i ncreased levels of stress hormone leads to reduced birth weight and adiposity in adulthood.
CRH is a hormone which usually leads to release of stress hormone. During pregnancy, most of the circulation CRH in the mother?s blood originates from the placen ta. The levels of circulating CRH are a good proxy of fetal exposure to maternal stress hormone. It has also been shown in humans that elevated levels of CRH in maternal blood correlates with low birth weight.
Adiponectin is a recently discovered hormon e produced by fat cells. It is inversely correlated with adiposity. In addition, studies have shown that this hormone plays an important part in regulating glucose and fat levels in plasma, as well as endothelial function and inflammation in humans.
Thu s, the aim of this project will be to study the association between maternal CRH-levels in pregnancy and offspring plasma adiponectin levels at 3 years.