Infant body composition relationship to maternal adipokines and fat mass: the PONCH study
Ulrika K Andersson-Hall1, Aldina Pivodic2,3, Hanna K de Maré2
1Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. ulrika.andersson.hall@gu.se.
Insights
Maternal leptin and its receptor influence infant fat in normal-weight mothers. For obese mothers, pre-pregnancy fat mass is key for infant fat accumulation. This highlights generational obesity programming factors.
Area of Science:
- Reproductive Biology
- Pediatrics
- Endocrinology
Background:
- Infant adiposity is linked to maternal fat mass and gestational weight gain.
- The role of maternal adipokines in infant adiposity is less understood.
- This study investigates maternal adipokines and fat mass in relation to infant adiposity.
Purpose of the Study:
- To determine how maternal leptin, soluble leptin receptor (sOB-R), adiponectin, and fat mass during pregnancy relate to infant fat mass.
- To compare these associations in normal-weight (NW) and obese (OB) women.
Main Methods:
- Longitudinal measurements of maternal body composition and serum adipokines (leptin, adiponectin, sOB-R) during pregnancy.
- Infant body composition assessed at 1 and 12 weeks postpartum.
- Study included 80 NW and 46 OB women.
Main Results:
- Maternal leptin and sOB-R levels increased during pregnancy.
- In NW women, infant fat mass was inversely associated with maternal leptin changes and sOB-R levels.
- In OB women, maternal fat mass was the primary determinant of infant fat mass at both 1 and 12 weeks postpartum.
Conclusions:
- Maternal leptin and sOB-R regulation impacts infant fat accumulation in normal-weight mothers.
- Maternal pre-pregnancy fat mass is a more significant factor than leptin in determining infant fat accumulation in obese mothers.
- Findings emphasize the importance of maternal factors in intergenerational obesity programming.
Background:
Infant adiposity is linked to both high maternal fat mass (FM) and excessive gestational FM gain, whereas the association with maternal adipokines is less clear. The aim was to determine how levels of maternal leptin, the soluble leptin receptor (sOB-R), adiponectin, and FM during pregnancy were linked to infant FM in normal-weight (NW) women and women with obesity (OB).
Methods:
Body composition and serum levels of leptin, adiponectin, and sOB-R were determined three times during pregnancy in 80 NW and 46 OB women. For infants, body composition was measured at 1 and 12 weeks of age.
Results:
Maternal leptin and sOB-R levels increased during pregnancy. For NW women, infant FM at 1 week was inversely associated with changes in maternal leptin and at 12 weeks inversely associated with absolute maternal sOB-R levels throughout pregnancy, as well as changes in sOB-R levels in early pregnancy. For OB women, infant FM at both 1 and 12 weeks were best explained by maternal FM.
Conclusions:
Leptin and sOB-R, thought to regulate leptin bioavailability, are associated with fat accumulation in infants born to NW women. In OB women, maternal FM in early pregnancy is more important than leptin in determining infant fat accumulation.
Impact:
In normal-weight women, the regulation of maternal leptin bioavailability during pregnancy has a role in infant fat mass accumulation. In women with obesity, however, pre-pregnancy maternal fat mass seems more important for infant fat mass. This is the first study of maternal adipokines and fat mass including longitudinal measurements in both mothers and their children. Understanding the relationship between maternal factors and infant fat mass is of great importance as obesity is programmed over the generations, and it is important to learn what regulates this programming.
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