Human placental lactogen and the diabetogenic state of pregnancy
Human placental lactogen (hPL), made by the placenta, makes the mother's tissues respond less to insulin, the diabetogenic state of pregnancy (a tendency towards the raised glucose of diabetes).
Remember
Human placental lactogen makes the mother insulin resistant, which keeps more glucose in her blood for the foetus. If her insulin response cannot keep up, gestational diabetes (diabetes first recognised in pregnancy) can follow.
Memory aid
Think of hPL as the placenta making the mother's cells 'deaf' to insulin: the sugar stays in her blood, so it is there for the baby to draw on.
Think of the mother's cells as unable to hear insulin, so glucose stays in her blood and is there for the baby.
Human placental lactogen acts on the mother, so its contribution to the foetus is indirect. Human placental lactogen (hPL) is a hormone made by the syncytiotrophoblast, the outer layer of the placenta, which makes its hormones. It acts on the mother's tissues so that they respond less well to insulin, the hormone that tells cells to take up glucose from the blood. This state is called insulin resistance.
Because her tissues take up less glucose, more of it stays in her bloodstream. Glucose reaches the foetus by facilitated diffusion (passive movement down a concentration gradient through carrier proteins), so a higher level in the mother's blood means more glucose is available to the foetus. The effect grows through the second half of pregnancy, when foetal demand is greatest. This tendency towards the raised glucose seen in diabetes is the diabetogenic state of pregnancy, and it is a normal adaptation, not a disease.
The key idea is resistance to insulin, not a lack of it. The mother's pancreas normally releases extra insulin to compensate, so her glucose usually stays within a safe range. If the pancreas cannot keep up, gestational diabetes (diabetes first recognised in pregnancy) can develop. Once the placenta is delivered, insulin needs fall quickly.
Other hormones of pregnancy have other roles. Progesterone promotes appetite and fat deposition, oestrogen regulates blood flow in the vessels supplying the placenta, and human chorionic gonadotrophin (hCG, the hormone detected by pregnancy tests) sustains the corpus luteum, the structure left behind after ovulation, in early pregnancy. Progesterone and cortisol also add to insulin resistance, but hPL is the placental hormone classically linked to it.
Key facts
- Source
- hPL is made by the syncytiotrophoblast of the placenta.
- Effect
- hPL causes maternal insulin resistance, so more glucose stays in the mother's blood for the foetus.
- Route to the foetus
- glucose crosses the placenta by facilitated diffusion, so a higher level in the mother's blood means more reaches the foetus.
- Timing
- insulin resistance rises considerably in the second half of pregnancy, and insulin needs fall quickly once the placenta is delivered.
- Limit
- if the pancreas cannot make enough extra insulin to compensate, gestational diabetes can result.
- Not alone
- progesterone and cortisol also contribute to insulin resistance in pregnancy, but hPL is the placental hormone classically linked to this effect.
Exam traps
- Human placental lactogen does not work by suppressing the mother's insulin secretion: the pancreas increases its insulin release to compensate, so the problem is a reduced response to insulin, not a shortage of it.
- Human placental lactogen does not make the mother's muscle more sensitive to insulin: that is the opposite of its real effect, since more glucose uptake into muscle would lower her blood glucose and leave less to cross to the foetus.
- Storing glucose in the placenta as glycogen would not raise the foetal supply, because the supply depends on the glucose level in the mother's blood, and it is hPL that raises that level.
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