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PubMed1975

Leukocyte alkaline phosphatase in newborn infants after delivery and in the puerperium.

Leukocyte alkaline phosphatase (LAP) activity increases progressively during pregnancy, returning to non-pregnant levels 6 weeks post-partum. This enzymatic activity is under the influence of placental steroid hormones, thus reflecting placental function. LAP activity is thus a reflection of the dynamic relations between estrogenic, progestational and corticoid activity during pregnancy. LAP activity was studied in 60 women and in their 61 newborn infants at delivery and during the first five days of the puerperium. The Kaplow cytochemical technique was employed. The average maternal LAP score as well as the average newborn infant LAP score was considerably higher than the LAP score of the normal adult. The level of the enzyme in the maternal granulocytes was significantly higher than that of the newborn (Tab. I). During the first five days after labor, there was progressive decrease in the LAP score in the maternal and the newborn blood; on the fifth day the LAP scores of both were only slightly above the normal adult score (Figs. 1, 2). An inverse relation between the LAP score and the birth weight of the infant was found (Tab. III). These results confirm the view that LAP activity in the fetus in utero, are dependent on placental steroid function. The lower LAP values in the newborn, as compared to those of the mother are probably dependent on the lower newborn hormone levels. The significance of the relation between LAP scores and the infants birth weight is not clear.

Alkaline Phosphatase↗
PubMed1984

[Dynamics of various peptide hormone receptors in human placental cell membranes].

The action of peptide hormone receptors on the cell membranes and the cyclic-AMP in its post receptor system dynamics was studied. [Results] Receptors for hCG-LH, hPL-hGH, ACTH and Insulin were found in the placental cell membranes but receptors for FSH and PRL were not found. The possibility was suggested that the cyclic-AMP was the second messenger in the receptor system for hCG-LH, hPL and ACTH. The differences between normal placental cell membranes and hydatidiform mole were studied from the point of view of the receptor level. Receptors on molar trophoblast for hCG-LH, hPL-hGH and ACTH increased about two fold to three fold over those on normal trophoblast. The presence of receptors for hCG-LH, hPL and ACTH was confirmed also in GCH-1 (gestational choriocarcinoma cell line). The possibility is shown that the placenta has an auto regularity system in its own tissue throughout the various peptide hormones receptors such as hCG-LH and hPL.

Chorionic Villi↗
PubMed1988

[Trophoblastic proteins].

Many studies conducted on human or animal placenta (chorion) suggest that the trophoblast is not only a passive filter between maternal and foetal blood flow, but is also endowed with complex functions. Factors of trophoblast origin involved in the mechanism of pregnancy recognition or maintenance of the progesterone environment required for the embryo survival, are reviewed. The main proteins involved in pregnancy are reported in table 1. Emphasis is laid on early signals of pregnancy which are of practical interest in human clinical medicine and animal husbandry. Among them, human chorionic gonadotropin (hCG), protein SP1 ("Schwangerschaftsprotein" 1) and some pregnancy-associated plasma proteins such as the PAPP A are very useful in the diagnosis of pregnancy, abortion, foetal abnormality or tumor in the human species. The presence of trophoblastin (presently studied in our laboratory) of a pregnancy-specific protein B and of early pregnancy factor (EPF) attest the establishment of pregnancy in domestic animals and in other mammals. The biological properties of some hormones such as placental lactogens (PL) or chorionic somatomammotropins (CS), human placental growth hormone (hPGH) contribute to a better understanding of the gestation function. Many other factors participate in the foetal development, for example, proliferin. Some proteins can display immunosuppressive properties or be responsible for the immune tolerance between the mother and the foetus. Although many placental proteins have already been defined, their biological functions have not yet been elucidated.

Animals↗
PubMed1996

Serial hematologic changes and pregnancy outcome.

OBJECTIVE: To reevaluate the concept that poor maternal hematologic changes relate to increased placental protein hormones, increased birth weight, and placenta to birth weight ratio. METHODS: Sixty-nine normal women were studied prospectively. On several occasions, pre-pregnancy, during pregnancy, and post-delivery, plasma volume was measured together with maternal hematologic indices and placental protein hormone levels. Birth weight and placental weight were measured at delivery. RESULTS: The decrements in hemoglobin concentration and hematocrit were apparent by 7 weeks' gestation. By 12 weeks, these progressive changes resulted mostly from the increase in plasma volume, and both hemoglobin concentration and hematocrit continued to decrease until near term. Increments in red cell and hemoglobin mass were maximal at 12-28 weeks of pregnancy. Concentrations of the placental hormones hCG and human placental lactogen at 12 weeks showed a lack of correlation with hemoglobin concentration or any other hematologic index. The correlations of birth weight with hemoglobin concentration and hematocrit at 36 weeks were not significant when we controlled for the effect of plasma volume. Neither hemoglobin mass at 36 weeks nor the change in hemoglobin concentration, hematocrit, and mean cell volume from the pre-pregnancy value to that at 36 weeks were significantly related to birth weight, placental weight, or the placenta to birth weight ratio. CONCLUSION: Low hemoglobin in late pregnancy reflects plasma volume changes, rather than poor maternal nutrition or adaptation, and is not linked to discordant placenta to birth weight ratio.

Confidence Intervals↗
PubMedDate not supplied

Biosynthesis, metabolism and regulation of steroid hormones secretion in the placental phase of gestation in the rat.

The regulation of biosynthesis of steroid hormones in the pre-placental stage and in placental phase of pregnancy in the rat is described. On the ground of our own studies a concept of an ovarian-placental unit in the rat has been formulated. This unit is characterized by coupled biosynthesis and secretion of steroid hormones in the placental stage of rat pregnancy.

Androgens↗
PubMed1989

Placental corticotropin-releasing hormone may be a stimulator of maternal pituitary adrenocorticotropic hormone secretion in humans.

To clarify the physiological role of placental corticotropin-releasing hormone (CRH), we measured plasma CRH, ACTH, and cortisol throughout pregnancy. Cerebrospinal fluid (CSF) CRH levels and ACTH responsiveness to synthetic CRH were also quantified in pregnant and nonpregnant women. Maternal plasma CRH levels, which increased progressively during pregnancy, correlated well with both ACTH and cortisol in early labor, delivery, and postpartum samples, and also with cortisol levels in samples before labor. CSF CRH levels in term pregnant women did not differ from those of nonpregnant women. CRH infusion that attained similar plasma CRH levels to those found in late pregnancy elicited significant ACTH release in vivo and regular CRH test provoked normal ACTH response during early pregnancy but no response during late pregnancy. We concluded that: (a) maternal pituitary-adrenal axis correlates well with plasma CRH levels, which are high enough to provoke ACTH release from maternal pituitary; (b) hypothalamic CRH secretion in term pregnant women is not exaggerated; and (c) maternal pituitary is responsive to synthetic CRH in early but not late pregnancy, suggesting that maternal pituitary-adrenal axis is already activated by high circulating CRH. Placental CRH may be an important stimulator of the maternal pituitary-adrenal axis during pregnancy.

Adrenocorticotropic Hormone↗
PubMed1998

Effect of betamethasone in vivo on placental corticotropin-releasing hormone in human pregnancy.

OBJECTIVE: The objective was to determine the effects of in vivo administration of prenatal betamethasone in patients at 26 to 35 weeks' gestation on corticotropin-releasing hormone concentrations in maternal and fetal plasma and amniotic fluid, and on corticotropin-releasing hormone localization in placenta and fetal membranes. STUDY DESIGN: A total of 49 pregnant women at risk for preterm delivery between 26 and 35 weeks' gestation were studied. Twenty-six patients received betamethasone (12 mg intramuscularly) for stimulation of fetal lung maturity. Cord blood, amniotic fluid, placental tissue, and fetal membranes were obtained from 22 of these patients at delivery by elective cesarean section at 33.8+/-2.4 weeks' gestation. In control patients (n=23) at comparable gestational age, blood samples were taken for hormone analysis (n=8), and cord blood, amniotic fluid, and tissues were collected at elective cesarean section at 34.1+/-2.3 weeks' gestation. Concentrations of corticotropin-releasing hormone, adrenocorticotropic hormone, and cortisol were determined by radioimmunoassay. Localization of tissue immunoreactive corticotropin-releasing hormone was assessed by immunohistochemistry. RESULTS: Betamethasone caused approximately 90% reduction in maternal cortisol and 50% reduction in maternal plasma adrenocorticotropic hormone. In patients at >30 weeks' gestation, there was a significant increase in maternal plasma corticotropin-releasing hormone concentrations after betamethasone; maternal corticotropin-releasing hormone was not altered significantly in untreated patients. Corticotropin-releasing hormone levels were raised in umbilical cord blood by 48 hours and in amniotic fluid 1 week after betamethasone administration. There was increased immunohistochemical staining for corticotropin-releasing hormone in placental syncytiotrophoblast and in fetal membranes of patients treated with betamethasone. CONCLUSIONS: These studies provide the first evidence for in vivo stimulation of plasma corticotropin-releasing hormone, likely of placental origin, by glucocorticoids in third trimester human pregnancy. The results suggest that increases in endogenous cortisol during normal gestation may contribute to placental corticotropin-releasing hormone output and to the rise in maternal plasma corticotropin-releasing hormone concentrations during late pregnancy.

Adrenocorticotropic Hormone↗
PubMed1983

Placental transfer and hormonal effects of metoclopramide.

In order to study the transplacental transfer of metoclopramide, and its endocrine effects, measurements were made of its concentration in maternal and fetal blood, and in the amniotic fluid, together with maternal and fetal plasma concentrations of prolactin, TSH and oestradiol, during delivery by selective Caesarean section. The drug, 10 mg, was injected i.m. 12 and 2 h and just before the onset of anaesthesia. Metoclopramide was detectable in all the umbilical arterial and venous and amniotic fluid samples, in mean concentrations of 50, 63 and 75 ng/ml, respectively. The mean ratio between the umbilical venous and maternal plasma concentrations was 0.63. Accurate maternal plasma half-lives could not be established but they must have averaged 2 to 4 h. The high amniotic fluid concentrations and relatively high umbilical venous and arterial concentrations soon after administration suggest that metoclopramide equilibrates relatively rapidly between the mother and fetus. Metoclopramide raised the maternal plasma prolactin levels from 315 +/- 128 ng/ml (SD) before therapy to 357 +/- 112 ng/ml at the time birth. No statistically significant difference in cord arterial or venous plasma prolactin levels was seen between the control and metoclopramide-treated groups. Metoclopramide did not affect maternal plasma TSH or oestradiol levels. The only change was a slight but significant increase in TSH level in cord blood taken from the umbilical artery after metoclopramide treatment.

Anesthesia, Obstetrical↗
PubMed1984

Gamma-glutamyltransferase activity in mammary gland of pregnant rats and its regulation by ovarian hormones, prolactin and placental lactogen.

Ovariectomy and ovariectomy plus hysterectomy on day 18 of pregnancy increased gamma-glutamyltransferase activity in the mammary gland. The withdrawal of progesterone and the subsequent release of prolactin are responsible for the rise in enzyme activity. Rat placental lactogen in the absence of prolactin and progesterone is able to induce gamma-glutamyltransferase activity.

Animals↗
PubMed1992

Radioimmunoassay of a bovine pregnancy-associated glycoprotein in serum: its application for pregnancy diagnosis.

A sensitive and specific double-antibody RIA for a bovine pregnancy-associated glycoprotein (bPAG) is described. The limit of detection was 0.2 ng/ml. The assay was specific for bPAG in that pituitary and placental gonadotropic hormones and other placental or serum proteins assayed in serial dilutions did not cross-react. The RIA allowed measurement of bPAG in placental extracts, fetal serum, fetal fluids, and serum or plasma of pregnant cows. About 20% of unbred heifers and nonpregnant cows had detectable levels ranging from 0.30 +/- 0.09 to 0.50 +/- 0.17 ng/ml (mean +/- SD), and 15% of bull sera showed higher concentrations (3.01 +/- 1.73 ng/ml) of bPAG or bPAG-like protein. Variations among animals was observed in fetal serum bPAG concentrations. Bovine PAG was detected in maternal peripheral blood at Day 22 of pregnancy (mean +/- SD, 0.38 +/- 0.13 ng/ml) in some animals and at Day 30 in all pregnant cows. Peripheral serum bPAG levels increased progressively to 3.60 +/- 1.73 ng/ml (mean +/- SD) at Day 30 of pregnancy, to 24.53 +/- 8.81 ng/ml at Day 120, and to 1551.91 +/- 589.68 ng/ml at Day 270. Peak concentration of bPAG was 2462.42 +/- 1017.88 ng/ml and it occurred 1-5 days prior to parturition. After delivery, bPAG concentrations decreased steadily to 499.63 +/- 267.20 ng/ml at Day 14 postpartum (pp), 10.12 +/- 7.84 ng/ml at Day 60 pp, and 1.44 +/- 1.08 ng/ml at Day 90 pp. The undetectable concentration (less than 0.20 ng/ml) was reached by Day 100 +/- 20 pp. An investigation undertaken in Holstein heifers, Holstein cows, and Hereford cows used as recipients for purebred Holstein embryos supplied evidence of the influence of breed of recipient and sex of fetuses on peripheral concentrations of bPAG. A herd of 430 Holstein-Friesian heifers that had received transferred embryos were bled at Day 35 postestrus (pe) for measurement of bPAG. The bPAG was detected in 287 of 430 serum samples analyzed. By rectal palpation performed at Day 45 pe, 267 heifers with detectable levels of bPAG at Day 35 pe were confirmed to be pregnant as were 3 of 143 heifers previously diagnosed as not pregnant by RIA. These results suggest that detection of this placental-specific antigen in the serum could be used as a specific serological method for early pregnancy diagnosis in cattle from 28 days after breeding.

Animals↗
PubMed2004

Endocrine profiles, haematology and pregnancy outcomes of late pregnant Holstein dairy heifers sired by bulls giving a high or low incidence of stillbirth.

The high incidence of stillbirth in Swedish Holstein heifers has increased continuously during the last 15 years to an average of 11% today. The pathological reasons behind the increased incidence of stillbirth are unknown. The present experiment was undertaken to investigate possible causes of stillbirth and to study possible physiological markers for predicting stillbirth. Twenty Swedish Holstein dairy heifers sired by bulls with breeding values for a high risk of stillbirth (n = 12) (experimental group) and a low risk of stillbirth (n = 8) (control group, group B) were selected based on information in the Swedish AI-data base. The experimental group consisted of 2 subgroups of heifers (groups A1 and A2) inseminated with 2 different bulls with 3.5% and 9% higher stillbirth rates than the average, and the control group consisted of heifers pregnant with 5 different bulls with 0%-6% lower stillbirth rates than the average. The bull used for group A1 had also calving difficulties due to large calves as compared to the bull in group A2 showing no calving difficulties. The heifers were supervised from 6-7 months of pregnancy up to birth, and the pregnancies and parturitions were compared between groups regarding hormonal levels, haematology, placental characteristics and calf viability. In group A1, 1 stillborn, 1 weak and 4 normal calves were recorded. In group A2, 2 stillborn and 4 normal calves were registered. All animals in the control group gave birth to a normal living calf without any assistance. The weak calf showed deviating profiles of body temperature, saturated oxygen and heart rates, compared with the normal living calves. No differences of the placentome thickness, measured in vivo by ultrasonography were seen between the groups. The number of leukocytes and differential cell counts in groups A1 and A2 followed the profiles found in the control group. In group A1, a slight decrease of oestrone sulphate (E1SO4) levels was found in the animal delivering a stillborn calf from the first 24-h blood sampling at 6 weeks to the second at 3 weeks prior to delivery, while the levels of E1SO4 at both periods in the animal delivering a weak calf followed the profile in animals delivering a normal living calf. During late pregnancy and at the time of parturition, the levels of E1SO4 and PAGs in animals delivering a stillborn or weak calf (from group A1) followed the normal profiles found in animals delivering a normal living calf. In group A2, low levels of E1SO4 and pregnancy associated glycoproteins (PAGs) over 24 h at both 3 and 6 weeks prior to parturition (< 1.5 nmol/L) were recorded in animals delivering a stillborn calf. During late pregnancy and parturition, the levels of E1SO4 and PAGs were slightly lower during 30-50 days prior to delivery and increased with a lower magnitude at the time of parturition. In conclusion, our results indicate that the aetiology behind stillbirth varies depending on the AI-bulls used and is associated with dystocia or low viability of the calves. Deviating profiles of oestrone sulphate (E1SO4) and pregnancy associated glycoproteins (PAGs) in animals delivering a stillborn calf not caused by dystocia were observed, suggesting placental dysfunction as a possible factor. The finding suggests that the analyses of E1SO4 and PAGs could be used for monitoring foetal well-being in animals with a high risk of stillbirth at term.

Animals↗
PubMed1995

Thyroid hormone regulates rat placental type III iodothyronine deiodinase activity by inducing kinetic changes different from those in the same isozyme in rat brain.

The kinetics of type III iodothyronine deiodinase (5-D) in rat placenta and brain and the role of phospholipids in enzyme activity were determined. Pregnant Sprague-Dawley rats were given either vehicle (control group) or T4 (15 micrograms/100 g bw/day; hyperthyroid group) from the 14th to the 21st day of gestation. Mitochondrial-microsomal fractions of the placenta and brain were used as the source of T4 5-D. Placental T4 5-D activity in the hyperthyroid group was increased when determined at 13 nM T4, but it was not significantly different from the control value when assayed at 1.3 microM T4. In contrast, T4 5-D in the brain was significantly increased in the hyperthyroid group regardless of the substrate concentration. Hyperthyroid rats showed decreased Km for placental 5-D and increased Vmax for brain 5-D. CM-Sephadex chromatography of solubilized placental microsomes was performed to determine whether phospholipids cause a reduction in the Km of placental 5-D in hyperthyroid rats. T3 5-D activity was undetectable unless protein-containing fractions were combined with phospholipid-containing fractions in the reaction mixture. Kinetic studies revealed that phospholipids had no effects on either Km or Vmax of placental T3 5-D. These data indicate that 5-D activity in the rat placenta is increased in hyperthyroidism with different kinetic changes from those in the brain, and that phospholipids have no effects on the kinetic parameters of placental 5-D whereas they are essential for the enzyme activity.

Animals↗
PubMed1984

The role of steroid hormones, prolactin and placental lactogen on mammary gland development in ewes and heifers.

In the first part of the investigations the interaction between oestradiol-17 beta, progesterone and prolactin on the formation of the lobuloalveolar structure of the mammary gland was studied in 21 nulliparous intact postpubertal ewes. Tissue specimens of the mammary gland were evaluated by light microscopical examination and prolactin was measured in blood samples. Combined treatment with oestradiol and progesterone induced physiological development of the lobuloalveolar structure of the mammary gland in the presence of prolactin. Suppression of prolactin by bromocriptine prevented this effect. Treatment with progesterone alone was not effective and revealed histological structures comparable to the controls. The interaction of oestradiol-17 beta with prolactin appears to be a main trigger for mammary gland development. In the second part of the investigations the effect of bromocriptine treatment during pregnancy on mammary gland development was studied in primigravid ewes and heifers. Mammary gland specimens were obtained for light and electron microscopical evaluation in ewes and heifers 5 and 10 days respectively before the expected date of parturition. Concentrations of prolactin and ovine placental lactogen were determined by radioimmunoassay. Bromocriptine treatment suppressed prolactin concentrations in ewes to minimal values but did not affect ovine placental lactogen concentrations. The histological evaluation revealed almost comparable stages of mammogenesis in both ewes and heifers. This effect can be attributed, at least in ewes, to the action of placental lactogen on mammogenesis. Placental lactogen might therefore be of physiological relevance during mammogenesis.

Animals↗
PubMed1980

Studies on the growth of the fetal sheep. The effects of reduction of placental size on hormone concentration in fetal plasma.

Intrauterine growth retardation was induced in sheep by removal of endometrial caruncles before pregnancy. At a second operation catheters were implanted into the ewe and fetus at 105-135 days of pregnancy. Three groups of fetuses: low birthweight-for-dates (small caruncle) normal birthweight-for dates (normal sized caruncle) and controls have been compared. The concentration of ACTH (60 +/- 6.9 pg/ml) in the normal-sized caruncle fetuses were lower in the controls (144 +/- 4.7 pg/ml) or small caruncle fetuses (142 +/- 53 pg/ml). Basal cortisol concentrations were similar in the controls (7.3 +/- 1.2 ng/ml) and normal-sized caruncle fetuses (6.5 +/- 0.5 ng/ml) but those in the small caruncle fetuses were significantly higher (12.7 +/- 1.0 ng/ml, P less than 0.001). The concentration of insulin correlated with plasma glucose and the mean concentrations were 19.2 +/- 1.6 mu units/ml (controls), 8.4 +/- 2.6 mu units/ml (normal-sized caruncle) and 3.9 +/- 1.6 mu units/ml (controls), 8.4 +/- 2.6 mu units/ml (normal-sized caruncle) and 3.9 +/- 1.6 mu units/ml (small caruncle). Prolactin was significantly lower in the small caruncle fetuses (2.1 +/- 0.3 ng/ml) compared to the controls (66.6 19.4 ng/ml) or normal-sized caruncles (76.1 +/- 38 ng/ml) but growth hormone concentrations in the small caruncle.

Adrenocorticotropic Hormone↗
PubMed2006

Peripartum maternal and foetal ghrelin, growth hormones, IGFs and insulin interrelations.

OBJECTIVE: Ghrelin may influence GH secretion and is associated with insulin sensitivity. In pregnancy, placental growth hormone (PGH) replaces GH. The aim of this study was to investigate the relationship between PGH and ghrelin and their relationship to insulin sensitivity in pregnancy. DESIGN: Prospective, descriptive study. PATIENTS: Thirty-seven singleton pregnant and six twin pregnant women MEASUREMENTS: Maternal blood samples were drawn before and 2 days after elective caesarian section (CS). Serum total ghrelin, PGH, GH, GH-binding protein, insulin and IGF-I and IGF-II, and plasma glucose were determined. Insulin sensitivity indices (ISIs) were calculated. Cord blood samples were drawn at delivery for ghrelin determination. RESULTS: Serum ghrelin only displayed a minimal, although statistically significant, decrease after CS. Prior to delivery serum PGH increased by 25% during fasting, and was undetectable the day after CS. Serum levels of GH were low until 48 h after CS. No significant correlations were detected between PGH or ghrelin and ISIs, although a trend was observed for ghrelin. Twin pregnancies had higher PGH levels than singletons; however, levels of IGFs were similar. In cord blood, ghrelin levels were higher in arterial than venous samples. CONCLUSIONS: Maternal ghrelin levels were only minimally affected by parturition, suggesting that maternal ghrelin is not involved in the transition from PGH to GH secretion. The increased arterial ghrelin levels in the foetus suggest foetal ghrelin production. Serum PGH appears to be influenced by fasting. Finally, elevated PGH levels in twin pregnancies do not appear to affect maternal IGF levels.

Adult↗
PubMed1986

Binding inhibition by monoclonal antibodies of ovine placental lactogen to growth hormone receptors in human liver.

In the radioreceptor assay for growth hormone (RRA-GH) using [125I]iodo-hGH, hGH and human liver membrane particulate fractions as tracer, hormone standard and receptors, respectively, ovine placental lactogen (oPL) is capable of inhibiting the binding of [125I]iodo-hGH in a parallel manner with hGH and in equipotency. Similarly, in the RRA-GH by employing [125I]iodo-oPL, oPL and human liver membrane particulate fractions as tracer, hormone standard and receptors, respectively, hGH is also equipotent as oPL in inhibiting the binding of [125I]iodo-oPL in a parallel fashion. The addition of monoclonal antibodies against oPL in the assay was effective in inhibiting the binding of [125I] iodo-oPL to human liver, but could not, however, inhibit the binding of [125I]iodo-hGH to human liver. Furthermore, the addition of the monoclonal antibodies in the RRA-GH did not affect the parallelism of the oPL standard but lowered the total binding of oPL. Our studies indicate that the structure of the binding sequence in oPL which binds to the GH receptor of human liver is not identical to the equivalent sequence of hGH and that the monoclonal antibodies compete with GH receptors in human liver for the binding of oPL.

Animals↗
PubMed1989

Role of carbohydrates in glycoprotein hormone signal transduction.

The structure of the polypeptide chains and oligosaccharide moieties of the alpha and beta subunits of pituitary and placental glycoprotein hormones are known. The dimeric polypeptide structure (but not the carbohydrate) is important for binding of the hormone to specific receptors. The N-linked but not O-linked carbohydrates, on the other hand, are required in some manner to activate the effector system. Hormones with depleted carbohydrate content (deglycosylated hormones) interact with receptor but are unable to activate intracellular events. Because of such discordant properties, these forms act as competitive inhibitors of hormone action. Through a combination of chemical deglycosylation procedures and site-directed mutagenesis, the first site of N-glycosylation from the NH2 terminus of the common alpha subunit has been identified to be more critical for glycoprotein hormone signal transduction. Control of glycosylation by the endocrine milieu could contribute to regulation of hormone function by secreting variable forms of agonist/antagonist.

Animals↗