Tag: excessive birth weight

  • The Essential Guide to Human Placental Lactogen in Pregnancy

    dr sanjana p

    Human placental lactogen is a peptide hormone secreted by the placenta during pregnancy. Additionally, it helps sustain pregnancy and supports breastfeeding. It also serves as a biomarker for pregnancy-related diabetes and for excess birthweight in babies.

    Human placental lactogen [hPL]

    Human placental lactogen is a hormone secreted by the placenta from the sixth week of pregnancy.

    Additionally, it has multiple roles in the body.

    It can sustain pregnancy raising the levels of estrogen and progesterone and prepare the breast milk ducts for breast feeding. Beyond all these roles ,its primary role is in glucose metabolism for growing fetus, as a constant source of energy.

    hPL also helps to grow milk glands in breasts making the mother’s body ready for breastfeeding. The hPL hormone promotes ductal and alveolar growth in the human mammary gland during the third trimester of pregnancy, in preparation for milk production.

    hPL rises steadily through gestation, and reaches its peak near the 34th week

    How does human placental lactogen affect glucose and fat metabolism in mother and fetus?

    Human placental lactogen has a crucial metabolic role.

    Moreover, it helps maintain glucose in the mother’s blood and influences birthweight of children.

    Human placental lactogen plays a pivotal role in maintaining glucose level in blood working against insulin. Insulin is the hormone secreted by beta cells of pancreas for promoting cellular uptake of glucose from the blood and provide glucose to cells. In normal conditions this blood glucose is taken up by body cells as primary source of energy. The insulin hormone facilitates this in non pregnant state. But once placenta starts secreting hPLhormone it sustains blood glucose levels high and directs it as a source of fuel for fetal growth.

     Here human placental lactogen in mothers facilitate presence of glucose in blood and it reaches fetal blood instead of being taken by maternal cells. Hence it may create an insulin resistance state elevating blood sugar level in mothers.  This function of hPL is ensuring free glucose delivery to fetal cells as source of energy.

      hPL saves glucose for baby and mother’s body may have to rely upon fat stores for energy. The stored maternal fats breakdowns into fatty acids as source of energy.

    Still there is obscurity regarding the conjoined role of other hormones in maintain blood sugar in mothers while hPL levels increase during third trimester of pregnancy.

    Th hPL hormone can be detected in pregnant women’s blood at approximately six week’s gestation. Thereafter the hPL levels begin to increase until the 30th week of pregnancy. By the third trimester of pregnancy it reaches the peak levels of 5000–7000 ng/mL. Roughly, the rate of secretion of hPL near the last term of pregnancy is about 1 g per day which is considerably higher.

    The higher late-pregnancy hPL is linked to gestational diabetes in mother and increased birthweight in the new born baby.

    Human placental lactogen – a predictive biomarker for fetal growth & birthweight

    In some women, during the last term of pregnancy the secretion of hPL may be abnormally high. The exact causes leading to this abnormal hormonal rhythm is still not fully understood. It is believed that hPL is regulated by several hormones conjointly.

    The spike or surge in last trimester or term of pregnancy gives some clues or indication about the excessive birth weight in the baby and gestational diabetes in women. Both are interconnected.

    hPL  hormone secretion disruptions outcome

    Obesity and diabetes during pregnancy is related to the hPL secretion pattern. Obesity is most often associated with lower hPL serum concentrations, diabetes results in increased hPL blood levels.

     Disruptions in hPL secretion by the placenta is linked with several issues during pregnancy such as placental dysfunction, diabetic retinopathy, and abnormalities in fetal growth &birthweight

    written by Dr. Sanjana p

    References