THYROID HORMONE – FUNCTIONS

B i.e. Thyroxine

A i.e. Thyroxine

B, C i.e. Insulin, Thyroxine

Ironically, fetal growth hormone does not appear to regulate growthQ, and anencephalic infants and GH-deficient children typically have normal birth weight.

–  Fetal thyroxine, insulin and glucocorticoidsQ play important role in intrauterine growth of fetus.

Placentral Hormones and Pregnancy

–  Endocrine function begins with the onset of implantation, when syncytiotrophoblasts start secreting the LH like protein hCG (human chorionic gonadot-ropin), which prevents I uteolysis (i.e. maintains the viability of corpus luteum) and thus maintains a high level of luteal derived progesterone production during the first 10 weeks. By this time (8-10 weeks), the syncytiotropholasts aquire the ability to make progesterone at sufficient levels to maintain pregnancy independently of corpus luteum (- referred to as luteal – placental shift) .

–  hCG has a a glycoprotein subunit (a-GSU) and a hormone specific 13-sub unit ((3-hCG). Antibody used to detect hCG in pregnancy tests and laboratory assay detect the 13 subunitQ. Being similar to LH, hCG binds with high affinity to LH receptors. But the 13 subunit of hCG is longer than that of LH & contains more sites for glycosylation, which greatly increase the stability (t₁₁₂ = 24-30 hours) allowing it to rapidly accumulate in maternal circulation such that the hCG is detectable within maternal serum within 24 hours of implantation.

–  Maternal serum hCG level doubles every 2 days for first 6 weeks & peak at about 10 weeks, then decline to a constant level at about 50% of the peak value. This rapid increase is responsible for the nausea of morning sicknessQ a/w early pregnancy.

–  Small (1-10%) amount of hCG enters fetal circulation and stimulate fetal leydig cells (to produce testosterone before fetal gonadotropic axis is fully mature) and fetal adrenal cortex.

Human placental lactogen (hPL) also k/a human chorionic somato mammotrophin (hCS) is a protein hormone (structurally similar to GH and prolactin /PRL) that is produced in syncytiotrophoblast. It can be detected within syncytiotrophoblast by 10 days after conception & in maternal serum by 3 weeks of gestation. Maternal level rises progressively during gestation (related to size of placenta). It is protein anabolic & lipolytic (like GH) and stimulates mammary gland growth & development (like PRL). Its antagonistic action to insulin is the major basis for diabetogenicity (insulin resistant state or accelerated starvation) of pregnancy. Mammary gland development in pregnancy results from action of hPL, PRL, estrogen & progestins. Both hPL & PRL act as fetal GHs & stimulate production of fetal growth promoting hormones insulin like growth factors (IGF) I & II.

Placenta (syncytiotrophoblast) also produce progesterone, estrogen and corticotropin releasing hormone (CRH). Progestore production by placenta is largely unregulated (i.e. produces as much as the supply of cholesterol & levels of CYP 11 Al & 3(3-HSD allow). Placental steroidogenesis differes from that in adrenal, cortex , ovaries & testis in that cholesterol is transported into the placental mitochondria by mechanism that is independent of St AR protein. This first step of steroidogenesis is not regulated, rate limiting step in placenta as it is in other steroidogenic glands. So fetus with inactivating mutation in StAR protein will develop hypogonadism, lipoid congenital adrenal hyperplasia but will produce normal progesterone levels by their placenta. Progesterone production by placenta does not require fetal tissue and are largely independent of fetal healthQ (i.e. cannot be used as a measure of feta health)Q.

Ans. A: Increased Thyroxine release

Thermoregulatory response activated by exposure to cold (via posterior hypothalamus).

• Increased heat production.
• Shivering.
• Hunger
• Increased voluntary activity.
• Increased TSH secretion.
• Increased catecholamine.
• Decreased heat loss.
• Cutaneous vasoconstriction.
• Curling up.
• Horripilation.
• Endocrine mechanisms that cause heat production (thermogenesis) are epinephrine, norepinephrine, and thyroxine (T₃ and T₄ regulation).
  • The production of thyroxine and triiodothyronine is regulated by thyroid-stimulating hormone (TSH), released by the anterior pituitary.
  • The thyroid and thyrotropes form a negative feedback loop: TSH production is suppressed when the T4 levels are high.
  • The TSH production itself is modulated by thyrotropin-releasing hormone (TRH), which is produced by the hypothalamus and secreted at an increased rate in situations such as cold exposure (to stimulate thermogenesis).
  • TSH production is blunted by somatostatin (SRIH), rising levels of glucocorticoids and sex hormones (estrogen and testosterone), and excessively high blood iodide concentration.