Serum Placental Lactogen Research Articles

Low serum placental lactogen at term is associated with postnatal symptoms of depression and anxiety in women delivering female infants

BackgroundPlacental endocrine insufficiency may increase the risk of depression and anxiety during pregnancy and/or after birth. This study investigated the association between serum human placental lactogen (hPL) and measures of perinatal mental health, accounting for selective serotonin-reuptake inhibitor (SSRI) usage. MethodCaucasian women with singleton, term pregnancies recruited at their pre-surgical appointment prior to an elective caesarean section (ELCS) were studied. Serum hPL levels were measured by ELISA in maternal blood collected at the pre-surgical appointment. Depression and anxiety scores were derived from Edinburgh Postnatal Depression Scale (EPDS) and the trait subscale of the State-Trait Anxiety Inventory (STAI) questionnaires completed at recruitment and three postnatal time points. Data was analysed by unadjusted and adjusted multiple linear regression. ResultsIn adjusted linear regressions, term maternal serum hPL levels were negatively associated with postnatal EPDS and STAI score ten weeks postnatal for mothers who had girls (B= -.367, p = .022, 95% CI -.679, -.056; and B= -.776, p = .030, 95% CI -1.475, -.077 respectively). Excluding women prescribed SSRIs strengthened the relationship at 10 weeks and uncovered an earlier association between hPL and mood scores within one week of delivery (EPDS B= -.357, p = .041, 95 % CI -.698, -.015; and STAI B= -.737, p = .027, 95 % CI -1.387, -.086). In mothers who had boys, there were no associations between hPL and mood scores at any time point. ConclusionLow hPL at term associated with postnatal depression and anxiety symptoms exclusively in mothers of girls. Insufficiency in hPL may contribute to maternal mood symptoms.

Effects of Genetic Selection for Milk Yield on Somatotropin, Insulin-Like Growth Factor-I, and Placental Lactogen in Holstein Cows

Cows from static, low-merit control (CL) and contemporary, high-merit select (SL) lines that differed in milk yield by more than 4,000 kg/305-d lactation (SL>CL) were used to determine effects of selection for milk yield on blood serum concentrations of somatotropin (ST), insulin-like growth factor (IGF-I), and placental lactogen (PL). Cows were exposed to the same environment and management conditions and fed the same diets. Serum and milk samples were collected from primiparous (18 CL, 18 SL) and multiparous (12 CL, 18 SL) cows relative to day of lactation (from −28 to 280 d for nonpregnant cows and to subsequent calving for cows that conceived). Data were analyzed as repeated measures using mixed model procedures. Serum ST increased at calving, remained elevated for a longer interval in SL than in CL cows, and was greater in SL than in CL cows. Serum IGF-I decreased at calving, remained low through 14 DIM, and gradually returned to precalving concentrations as lactation progressed. Postpartum concentrations of IGF-I were less in SL than CL through 84 DIM and were similar through the remainder of lactation, resulting in a line by day interaction. Serum IGF-I and PL were not affected by merit during gestation. There was an interaction of merit and postconception interval on IGF-I, with the difference in IGF-I concentration between lines decreasing as gestation progressed. Change in serum IGF-I and PL appeared to be synchronous. Results indicate that selection for milk yield increased serum ST, prolonged the postpartum reduction in serum IGF-I, and did not alter serum PL. Results also indicate a positive relationship between PL and IGF-I and support the concept that PL plays a role in the regulation of serum IGF-I during gestation.

Serum concentrations of insulin-like growth factors and placental lactogen during gestation in cattle. II. Maternal profiles

This study was designed to examine the effects of fetal growth potential on maternal hormones and lipid metabolism. Sixty beef heifers were inseminated with semen from sires with high (H) or low (L) expected progeny differences for birth weight. Maternal serum was collected at 21-d intervals from Day 85 to Day 274 of gestation. Serum concentrations of insulin-like growth factor (IGF)-I, IGF-II, placental lactogen (PL), and nonesterified fatty acids (NEFA) were determined and correlated to fetal and maternal characteristics. Maternal serum IGF-I declined throughout pregnancy, whereas IGF-II was relatively constant and PL tended to increase. Maternal serum NEFA was low and invariant through Day 211 of gestation when it rose 3.5 times to peak levels at Day 253 and declined at Day 274. PL was positively correlated to NEFA (r = 0.37, P < 0.01), IGF-I was negatively correlated (P < 0.01) to NEFA and PL (r = −0.59, and −0.35, respectively), and IGF-II was negatively correlated to NEFA (r = −0.35, P < 0.01). Dams pregnant with H fetuses had lower (P = 0.02) serum IGF-I and tended to have higher (P = 0.09) serum PL concentrations than dams carrying L fetuses. Additionally, dams pregnant with L fetuses had higher (P < 0.03) serum IGF-II concentrations than dams with H fetuses (175.6 vs. 145.0 ng/ml) during the third trimester. Fetal sex had no effect on any maternal serum parameter. Fetal weight and instantaneous growth rate (IGR) were positively correlated to maternal NEFA and PL and negatively correlated to maternal IGF-I and IGF-II. Independent IGR effects were detected for PL (P < 0.06) and IGF-I (P < 0.0005) concentrations. Maternal hip height was negatively related to serum IGF-I and positively related to serum PL concentrations. Maternal body weight and body condition score were correlated with several serum parameters but were confounded by day of gestation. Correlation analysis of serum concentrations of IGF-I, IGF-II, and PL did not support the hypothesis that PL regulates IGF concentrations.

Serum concentrations of insulin-like growth factors and placental lactogen during gestation in cattle I. Fetal profiles

Sixty crossbred beef heifers pregnant with fetuses of either high (H; n = 30) or low (L; n = 30) genetic potential for growth were used to establish fetal serum profiles of insulin-like growth factor (IGF)-I, IGF-II, and placental lactogen (PL), and to examine relationships between serum hormone concentrations and fetal growth parameters. Three H and three L fetuses were collected by caesarean section at 21-d intervals from Day 85 through Day 274 of gestation. Arterial, venous, and mixed umbilical blood samples were collected during surgery. Fetal body weight, crown-rump length, hip height, and heart girth were measured. Serum concentrations of IGF-I and IGF-II increased (P < 0.0001) with advancing gestational age, whereas serum PL declined (P < 0.0001) linearly (P < 0.01) throughout gestation. Serum concentrations were greater in the umbilical vein compared with the umbilical artery for IGF-11 (P < 0.0001) and PL (P < 0.05), but not IGF-1. Fetal IGF-I, IGF-II, and PL serum concentrations were not correlated with serum concentrations of the respective maternal hormones. Fetal serum IGF-I concentrations were correlated to fetal body weight (r = 0.66), growth rate (r = 0.72), crown-rump length (r = 0.20), hip height (r = 0.17), and heart girth (r = 0.20). Correlations between fetal serum IGF-11 concentrations and the same parameters were 0.60, 0.62, 0.39, 0.34, and 0.37, respectively. Fetal serum PL concentrations were negatively correlated to body weight (r = −0.40) and growth rate (r = −0.40) and not correlated with any fetal linear measure. Fetal genotype (L vs. H) differences were detected for IGF-I (P < 0.05) and PL (P = 0.09) concentrations. Fetal sex effects were not observed for any hormone. Maternal sire breed, hip height, and body condition score did not influence fetal serum hormone concentrations.

Women with prolactin-producing pituitary adenoma show decreased serum placental lactogen during pregnancy.

Prolactin (PRL), growth hormone (GH), placental lactogen (PL), chorionic gonadotropin (CG), estradiol (OE), progesterone (P4) and sex hormone-binding globulin (SHBG) were measured in serum throughout gestation in 9 women with PRL-producing pituitary adenomas. They had been treated at least 1 year with the dopamine agonist bromocriptine before pregnancy occurred. All women bore healthy babies of normal birthweight. Their PRL levels did not show the successive increase seen in normal pregnancies; serum PRL was unphysiologically increased in all patients up to the 20th week of gestation, whereafter PRL levelled off and fell within the normal range. Serum PL levels were lower in the women with prolactinoma compared to healthy pregnant women, despite normal placental weight. The serum GH levels in the patients determined with an immunoassay based on a monoclonal antibody, were low or nondetectable, similar to healthy pregnant controls. In contrast, high molecular weight GH in serum as determined with a monoclonal antibody which also recognizes PL appeared to be increased in comparison with healthy pregnant women. The serum levels of CG, OE, P4 and SHBG were all within the normal range. These results show that the unphysiological secretion of PRL in pregnant women with PRL-producing pituitary adenomas is associated with decreased serum levels of PL.

Involvement of the adrenergic system on the release of prolactin and lactogenesis at the end of pregnancy in the rat

The part played by the adrenergic system on the release of prolactin and lactogenesis induced by prostaglandin F2 alpha and the antiprogesterone RU 486 was studied in pregnant rats. Two doses of prostaglandin F2 alpha (150 micrograms) administered at 08.00 and 12.00 h on day 19 of pregnancy induced, at 12.00 h on day 20 (24 h after administration), a significant increase in the serum concentration of prolactin, with a significant decrease in serum progesterone levels. These hormonal changes significantly augmented casein and lactose levels in the mammary gland. Treatment with RU 486 (2 mg/kg) at 08.00 h on day 19 augmented casein and lactose concentrations in the mammary gland at 12.00 h on day 20 without modifying serum concentrations of prolactin and progesterone. The adrenergic antagonists, propranolol (3 mg/kg), metoprolol (10 mg/kg), ICI 118,551 (200 micrograms/kg), idazoxan (100 micrograms/kg) and prazosin (10 mg/kg), were administered s.c. at 12.00 and 20.00 h on day 19 and 08.00 h on day 20 of pregnancy to intact rats or to rats previously treated with RU 486 or prostaglandin F2 alpha. These adrenergic antagonists did not modify serum prolactin or progesterone levels in intact or RU 486-treated rats, but serum prolactin levels in the prostaglandin F2 alpha-treated group were significantly reduced by treatment with propranolol, metoprolol or prazosin. In addition, propranolol and ICI 118,551 also decreased the casein and lactose concentrations in the mammary glands of RU 486- and prostaglandin F2 alpha-treated rats, while the other compounds had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Comparison of serum placental protein hormone levels in diabetic and normal pregnancy.

Conflicting data exist concerning maternal serum concentrations of placental hormones during pregnancy in women with diabetes mellitus. To resolve some of these discrepancies, women participating in the NICHD-Diabetes in Early Pregnancy Study were studied. In this collaborative study, pregnancy was identified within 21 days of conception by serum hCG measurements. We prospectively collected 185 blood samples from 35 insulin-dependent diabetic women and 166 blood samples from 31 control women, all between 5 and 37 weeks gestation. Serum concentrations of hCG, pregnancy-specific beta-1-glycoprotein, placental lactogen, and hCG alpha were measured serially. The relationship between serum hormone, fasting blood glucose, 1-h postprandial blood glucose, and glycosylated hemoglobin concentrations was compared. Serum hCG alpha levels were significantly lower in the diabetic women than in control women at multiple time points during the first and second trimesters, while no consistent differences in the serum concentrations of hCG or pregnancy-specific beta-1-glycoprotein were found between pregnant diabetic and control women. Serum placental lactogen levels were significantly lower in diabetic women at 9-10 weeks and 20 weeks gestation. There were no correlations between fasting blood glucose, 1-h postprandial blood glucose, or glycosylated hemoglobin and any of the placental protein levels in the diabetic women. These data are consistent with a defect in synthesis and/or secretion of hCG alpha by the cytotrophoblast during the first two trimesters of pregnancy in insulin-requiring diabetic women.

Maternal serum placental lactogen and α-fetoprotein in smokers: Relationship to placental weight and birth weight

SummaryIn a study of light to moderate smokers (1 to 14 cigarettes per day; n = 485), heavy smokers (15 or more cigarettes per day; n = 334) and non-smokers (n = 1814) smoking in pregnancy was associated with smaller birth weights and occipito-frontal circumferences in the new-born together with smaller placental weights. Serum α-fetoprotein and placental lactogen were measured at 16 weeks and 32 weeks of pregnancy respectively. Both placental lactogen and α-fetoprotein levels were higher with greater consumption of cigarettes. Placental lactogen increments in both smokers and non-smokers were associated with greater placental weight, birth weight, and occipital-frontal circumference. By contrast, higher α-fetoprotein levels were associated with lower placental weight, birth weight and occipito-frontal circumference in both non-smokers and smokers. Because maternal α-fetoprotein is higher with increased cigarette consumption, smoking may cause damage to the placenta and release of α-fetoprotein into the m...

The effect of hypophysectomy on serum placental lactogen and progesterone in the mouse.

Hypophysectomy of pregnant mice on days 10, 12, and 16 of gestation resulted in a large and rapid (12-24 h postoperatively) increase in serum placental lactogen (mPL) concentrations, as measured by homologous RIA. Serum progesterone (P4) concentrations decreased compared to those in intact and sham-operated controls. Significantly, the increase in serum mPL in mice hypophysectomized on days 10 and 12 preceded any decrease in serum P4 concentrations by at least 24 h, suggesting that two indirectly related mechanisms may be involved in the control of the serum concentrations of these hormones. The weight of the uterus, including the feto-placental units, placental weight, and placental content of mPL did not differ between intact, sham-operated, and hypophysectomized groups. The gestational profiles of serum GH and PRL concentrations were similar in the sham-operated and intact controls. Although serum P4 concentrations decreased after hypophysectomy on days 10 and 12 of gestation, the maintenance of the pregnancy was not affected; thus, the reduced concentrations of serum P4 (approximately 50% of control by day 16) were adequate to allow the pregnancy to continue. Hypophysectomy on day 16 of gestation resulted in spontaneous abortion 48 h postoperatively in all but one animal. We conclude that the absence of some pituitary factor(s) results in a rapid increase in serum mPL, while a concomitant, albeit gradual, decrease in serum P4 begins 48 h postoperatively. Therefore, when the pituitary no longer contributes to the luteotropic complex of the midpregnant mouse, an increase in serum mPL alone cannot maintain serum P4 concentrations at control values.

301 SOMATOMEDIN-C (SM-C) LEVELS IN FETAL SHEEP ARE INDEPENDENT OF SERUM PLACENTAL LACTOGEN LEVELS

The factor(s) regulating fetal growth remain obscure and classic hormones appear not to be involved. Fetal size correlates with fetal SM-C levels; however, fetal growth hormone appears to have no effect either on fetal SM-C or fetal growth. Placental lactogen has been suggested as a modulator of fetal somatomedins. To assess this possibility in the sheep model, time-dated pregnant ewes with singleton fetuses (n=7) underwent fetal arterial catheterization at 111±3 d of gestation (term=150 d). Daily blood samples were obtained from each fetus until parturition or death. (Mean survival=20 d). Serum samples were assayed for both placental lactogen and SM-C. There was no correlation between placental lactogen and SM-C during the study period (r=.03, n=82). A second group of fetuses (n=5) underwent single umbilical artery ligation at 111±3 d of gestation. This procedure results in markedly elevated levels of placental lactogen in the fetus. Chronically catheterized animals were sampled daily and samples were assayed for both placental lactogen and SM-C. Despite the increased plasma placental lactogen levels in these single umbilical artery ligated fetuses, there was no demonstrable correlation between plasma placental lactogen and SM-C concentrations (r=.03, n=66).Conclusion: Somatomedin-C levels in fetal sheep are independent of serum placental lactogen levels during the third trimester.

Placental lactogen secretion in the mouse: in vitro responses and ovarian and hormonal influences.

In vivo and in vitro methodologies were utilized to study the regulation of placental lactogen (PL) secretion in the mouse. Chorioallantoic placental explants obtained from midpregnant (day 10 of gestation) C3H/HeN or Swiss Webster mouse conceptuses behaved differently in culture than explants of chorioallantoic placentas obtained later in pregnancy. Midpregnant placental explants maintained or showed an increasing amount of PL output per day for 5-6 days of culture, while gestationally older placental explants demonstrated a progressive decline in PL output per day over the 5-6-day culture period. On selected days of gestation, bilaterally ovariectomized C3H/HeN or Swiss Webster mice were shown to have significantly higher serum PL concentrations than sham operated mice. Reduction of serum progesterone concentrations by unilateral ovariectomy and/or partial lutectomy had no significant effect on serum PL concentrations. Progesterone significantly reduced PL production by midpregnant placental explants from both C3H/HeN and Swiss Webster mice, whereas 17 beta-estradiol did not significantly affect PL release in vitro. PL production by mouse chorioallantoic placentas has gestational specific characteristics in vitro and is responsive to regulatory influences of the maternal ovaries and progesterone.

Which is the best placental function test? A comparison of placental lactogen and unconjugated oestriol in the prediction of intrauterine growth retardation

Serum placental lactogen (hPL) and unconjugated oestriol (E3) levels were measured in 392 women at weekly intervals from 36–40 wk gestation. The levels of both hPL and E3 were reduced in subjects delivering a growth-retarded child. The clinical significance of this observation was similar for the two compounds, with a marginal advantage to hPL. There was a higher incidence of falling levels of hPL and E3 in cases of growth retardation but the finding had very little predictive value in an individual patient.

Human placental lactogen in pre-eclampsia.

Serum placental lactogen (hPL) was measured in serial blood samples obtained from 663 pregnant women at weekly intervals from 36 to 40 weeks. The group included 231 women with pre-eclampsia. Levels of hPL were significantly elevated in primigravidae with this condition but not in multigravidae. In all groups hPL levels were significantly reduced in association with growth retardation, but the clinical value of this observation appeared to be greater in multigravidae than in primigravidae. It is suggested that in primigravidae with pre-eclampsia maternal hPL levels reflect both the pathology of the disease as well as the condition of the fetus.

Ovariectomy leads to a rapid increase in rat placental lactogen secretion.

Serum placental lactogen (rPL) levels were measured by RIA in late pregnant rats subjected to a number of endocrine ablations. Adrenalectomy or unilateral ovariectomy had no significant effect on serum rPL levels. Hypophysectomy of the dam at midpregnancy resulted in a significant increase in serum rPL at late pregnancy. Bilateral ovariectomy of day-14 or -16 pregnant rats led to a rapid increase in serum rPL levels for 2 days followed by a gradual decrease as fetuses were reabsorbed or aborted. Adrenalectomy combined with ovariectomy led to sustained, elevated levels of serum rPL which were greater than those seen with bilateral ovariectomy alone. When progesterone (4 mg/rat X day) and estrone (500 ng/rat X day) or 17 beta-estradiol (100 or 200 ng/rat X day) were administered to ovariectomized pregnant rats, serum rPL remained elevated and the conceptuses were retained. In conclusion our studies have shown that ovarian and adrenal factors influence rPL secretion.

Protein Deficiency in Pregnant Rats Causes Decreased Levels of Plasma Somatomedin and Its Carrier Protein Associated with Reduced Plasma Levels of Placental Lactogen and Hepatic Lactogenic Receptor Number

Rats were fed either a 20% lactalbumin (control) or a 5% lactalbumin (low protein) diet for the last 2 weeks of pregnancy. At day 20 of gestation, rat serum placental lactogen levels, measured by radioreceptor assay, were significantly decreased by the low protein diet, thus confirming our earlier findings. The number of microsomal membrane lactogenic receptors, measured on the maternal livers at the end of pregnancy, was severely reduced in the livers of the low protein group, whereas protein deficiency did not affect binding affinity. Serum concentrations of somatomedin, measured by a competitive binding assay after acid treatment of the serum to remove endogenous carrier protein, were extensively reduced in the low protein group. The amounts of the somatomedin carrier proteins in the serum were assayed by separation on Sephacryl-S300 columns into higher- and lower-molecular-weight fractions peak 2 and peak 3, respectively. For the low protein diet group, both fractions showed a reduction in binding capacity, more marked in the case of peak 2. Since placental lactogen is known to influence output of somatomedin by the liver, we hypothesize that protein deficiency during pregnancy causes a fall in serum somatomedin level by reducing secretion of placental lactogen, which regulates its production by the liver.

In Vitro Follicular and Luteal Steroidogenesis in the Pregnant Hamster with Preliminary Studies in the Rat

Serum levels of progesterone (P4), 17 alpha-hydroxyprogesterone (17-OHP), androstenedione (delta) and estradiol (E2) reached their zenith on Day 14 of hamster pregnancy but were not associated with increases in serum pituitary gonadotropins or placental lactogen (Day 1 = day of sperm in vaginal smear). Steroid levels declined drastically on Day 16-the day of delivery. When follicles from proestrous hamsters (0900 h) were incubated for 1 h, E2 was accumulated in the medium at about twice the levels produced by follicles from pregnant animals except on Day 8 of gestation, when the values were about the same as for proestrus and on Days 12 and 16 when E2 was usually undetectable. Addition of 100 ng luteinizing hormone (LH) for 1 h showed that the proestrous follicle was considerably more active in E2 production than any of the follicles of pregnancy, with maximal stimulation in the latter group observed on Day 8 and minimal responsiveness on Day 16. An inverse relationship existed between the patterns of follicular production of P4 and 17-OHP versus delta and E2. Thus, during the baseline incubation, the proestrous follicle accumulated much less P4 than E2 in comparison to the situation during pregnancy. When stimulated by LH, maximal follicular production of P4 was on Day 16 of pregnancy when conversion to E2 and delta was minimal. Although the pathway from C21 to C18 steroids was "open" at all times for the hamster follicle during pregnancy, the rate at which P4 was converted to E2 varied at different stages of gestation. Corpora lutea (CL) from pregnant hamsters were incubated for 1 h to determine the amount of steroids accumulated in the medium. The CL were capable of producing steroids from P4 through E2 except on Day 16 when the levels for all steroids were very low. When 10 ng delta or testosterone were added as substrate, luteal E2 accumulation was greatly increased with peak conversion on Days 12 and 14 of pregnancy. Luteal and follicular function were compared for rats and hamsters on Day 8 of pregnancy. The CL of both species produced E2 per CL, to the same extent in the absence or presence of testosterone. The rat follicle in the baseline incubation accumulated 8X as much P4 and one-fifth as much E2 as the hamster. When stimulated by LH, the rat follicle did not increase the accumulation of E2 or delta over baseline levels but there was a striking increase in P4 (8 ng/follicle). Possible reasons for altered steroidogenesis during pregnancy are discussed.

Genetic and litter size effects on serum placental lactogen in the mouse.

Placental lactogen (PL) and progesterone are important hormones of pregnancy in the mouse. The purpose of this study was to investigate the influence of genetic differences and litter size on serum PL levels in the mouse. Serum progesterone levels were also measured in some experiments. Two features of serum PL levels under genetic control were identified: 1) the gestational profile of serum PL and 2) absolute serum PL levels. Breeding combinations that resulted in profound effects on serum PL levels were without significant affect on serum progesterone levels. Serum concentrations of PL and progesterone were directly proportional to litter size. Conceptus number was found to significantly affect ovarian progesterone release. The presence of uterine tissue antagonized the luteotropic actions of the conceptus but did not affect serum PL levels.

Adipose tissue metabolism during early pregnancy in the rat: Temporal relationships of changes in the metabolic activity, number of insulin receptors, and serum hormone concentrations

The temporal relationships between changes in rates of fatty acid and acylglycerol glycerol synthesis; the activity of lipoprotein lipase of parametrial adipocytes and their capacity to bind insulin; and the serum concentrations of insulin, progesterone, prolactin, and total lactogenic activity have been examined in rats during the first 15 days of pregnancy. The rate of fatty acid and acylglycerol synthesis showed a transient increase at Days 9 and 12 of pregnancy, whereas there was no change in the activity of lipoprotein lipase activity except for a fall between Days 12 and 15 of pregnancy. The capacity of adipocytes to bind insulin was increased by Day 6 of pregnancy and remained elevated until at least Day 15; no changes in the affinity for insulin were observed. Serum progesterone, insulin, and total lactogenic activity were elevated by Days 3, 9, and 12 of pregnancy, respectively. The results show that progesterone but not placental lactogen could be responsible for the rise in the insulin-binding capacity of rat adipocytes during pregnancy, whereas the fall in lipogenic capacity at about Day 12 of pregnancy coincides with the rise in serum placental lactogen.

What do placental function tests predict? Observations on placental lactogen levels in growth retardation and fetal distress

Single blood samples were obtained from an unselected population of 527 women between 36 and 40 wk gestation. Serum placental lactogen levels were lower than normal in patients whose infants were growth retarded or developed fetal distress in labor. These associations were independent; the fetal distress group did not contain an excess of subjects with growth retardation. Thus, the results of a biochemical test reflect dynamic aspects of placental function and not simply the overall growth of fetus and placenta.

Human placental lactogen and pregnancy-specific beta 1-glycoprotein in pregnant diabetic women.

Serum placental lactogen (hPL) and pregnancy-specific beta 1-glycoprotein (SP1) concentrations were measured in 16 insulin-dependent pregnant diabetic women and in 16 non-diabetic control subjects matched for placental weight. hPL concentrations were found to be significantly higher in diabetics with placental weight greater than 90th centile compared with those in (i) non-diabetic controls with placental weight greater than 90th centile and (ii) diabetics with placental weights less than 90th centile. SP1 concentrations were higher in both diabetic groups compared with those in their respective non-diabetic controls, but no difference existed between the two diabetic groups. In the control subjects infant birthweights were lower in the women with small placentae, but no such difference was observed between the two diabetic groups.