Placental lactogen Some species –Type of placentation Ruminants Humans Rodents Produced by fused cells –Syncytiotropoblast –Binucleated/trinuclea ted cells

Proteins related to pituitary GH and prolactin –Close to GH in humans –Close to prolactin in rodents –50-50 in cows

Function –Regulation of metabolism GH-like activity –Much weaker than pituitary GH –Development of mammary gland Prolactin-like activity –Maintenance of CL function Rodents during early stage of pregnancy

No known receptor(s) for placental lactogen –Interacts with GH receptor –Interacts with prolactin receptor

Pattern of secretion –Different between cattle and sheep Degree of fusion between tropoblasts and endometrium

GH-Variant –Human only –Acts like GH Tissue growth Nutrient metabolism –Affects function of insulin Pregnancy-induced diabetes

Placental steroidogenesis Cholesterol –Lipoproteins from circulation No De Novo synthesis Progesterone –Replace CL in some species Maintenance of pregnancy Precursor for fetal adrenal steroids

Estrogens –Limited production Limited 17  -hydroxylase activity –Abundant in fetal adrenal gland –Androgens from fetal adrenal gland Converted to estrogens in the placenta –Production of estriol rather than estradiol –Secretion of estrone Majority of placental estrogen in some species

Parturition Three stages –First stage Initiation of myometrium contraction Initiated by the fetus –Second stage Expulsion of the fetus –Third stage Expulsion of fetal membrane

Parturition First stage –Initiated by fetus –Distress Maximum size that can be maintained –Lack of nutrients –Hypoxia Activation of fetal hypothalamus-pituitary- adrenal axis –Release of ACTH by the fetal pituitary gland

Fetal ACTH –Release of cortisol from fetal adrenal gland Fetal cortisol –Removal of “progesterone block” Contraction of myometrium Conversion of progesterone to estradiol –17a-hydroxylase –17-20 lyase –Aromatase

Fetal cortisol –Increase production of PGF2a by the endometrium Further removal of progesterone block –Cause luteolysis Stimulates contraction of myometrium –Synergism with estradiol

Contraction of myometrium –Pushes the fetus toward cervix Activation of the CNS –Secretion of oxytocin from the posterior pituitary gland Oxytocin –Increased contraction of the uterine smooth muscle –Positive feedback More contraction (pushing of fetus), increased oxytocin secretion Entering of the fetus in the cervical canal –End of the first stage

Expulsion of fetus Relaxation of the cervix and pelvic ligaments –Relaxin Secretion stimulated by PGF 2 

Role of estradiol on parturition –Increased overall secretory activity Mucus production by cervix and vagina –Removal of cervical plug –Lubrication

Rupture of fetal membrane –Loss of amniotic and allantonic fluid Further lubrication Fetus becomes hypoxic –Movement of the fetus Stimulates further contraction of the myometrium –Increased strength of contraction

Expulsion of the fetal membrane Shortly after expulsion of the fetus –Dislodging of fetal membrane from the uterus –Vasoconstriction

Mammary gland development Cyclic changes in ovarian steroid hormones –Essential for mammary development Estradiol –Development of mammary alveoli (secretory unit) Progesterone –Development of mammary ducts

Final stage of mammary gland development –Pregnancy Ovarian/placental steroid hormones –Periparturient period GH and prolactin –Placental lactogen? Glucocorticoids

Lactation Parturition –Metabolic shift Fetal growth to synthesis and secretion of milk –Mobilization of nutrients Storage within the body –Fats Triggered by changes in hormones

Lactation and re-initiation of reproductive cycle Lactating women –High prolactin –Low LH and estradiol No ovulation –Lactation-induced anovulation/amenorrhea (infertility) –Women remain anovulatory as long as they breast-feed their babies Increased survivability of the infants

Lactational anestrus in the domestic species –Divert nutrients for lactation Ensure the survival of offspring –Lactation stimuli/physical contact between mother and offsprings –Animals remain in anestrus (absence of estrus) until nutrient intake exceeds nutrient demand