Prolactin receptor gene expression and foetal adipose tissue

Area of Science:

• Reproductive biology
• Developmental programming
• Endocrinology

Background:

• Fetal adipose tissue development is crucial for postnatal adaptation.
• Prolactin receptor (PRLR) gene expression in adipose tissue is not well understood during fetal development.
• Gestational factors like nutrition and placental function can influence fetal growth and development.

Purpose of the Study:

• To investigate the impact of increasing gestational age, maternal undernutrition, and restricted placental growth on PRLR gene expression in fetal sheep perirenal adipose tissue.
• To determine the role of prolactin in fetal adipose tissue development.

Main Methods:

• Collected perirenal adipose tissue from fetal sheep at various gestational ages (90-145 days).
• Utilized ribonuclease protection assays to quantify messenger RNA (mRNA) for PRLR long (PRLR1) and short (PRLR2) forms, and glyceraldehyde-phosphate-dehydrogenase (GAPDH).
• Manipulated fetal nutrient supply through placental restriction or maternal feed restriction.

Main Results:

• Perirenal adipose tissue mass and PRLR1/PRLR2 mRNA abundance increased significantly between 90 and 125 days of gestation, then declined by 145 days.
• Both placental restriction and maternal undernutrition reduced fetal adipose tissue deposition.
• Placental restriction decreased PRLR1 mRNA abundance, while maternal undernutrition did not affect PRLR1, PRLR2, or GAPDH mRNA levels.

Conclusions:

• PRLR gene expression is closely linked to the period of rapid fetal adipose tissue deposition.
• Prolactin signaling likely plays a significant role in the growth and maturation of fetal adipose tissue before birth.
• The effects of nutritional challenges on PRLR gene expression differ between placental restriction and maternal undernutrition.