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 Table of Contents  
Year : 2021  |  Volume : 12  |  Issue : 5  |  Page : 66-72

Serum human placental lactogen and prolactin may not be associated with aberrant glucose homeostasis in GDM

Department of Endocrinology, Bangabandhu Sheikh Mujib Medical University, Shahbag, Dhaka, Bangladesh

Date of Submission23-Mar-2021
Date of Decision18-Apr-2021
Date of Acceptance28-Apr-2021
Date of Web Publication20-Jul-2021

Correspondence Address:
Prof. Muhammad Abul Hasanat
Department of Endocrinology, Room No 1524, D-Block, Bangabandhu Sheikh Mujib Medical University, Shahbag, Dhaka.
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jod.jod_111_20

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Background: Gestational diabetes mellitus (GDM) shows insufficient β-cell compensation for insulin resistance (IR) during late pregnancy, whereupon derangements of human placental lactogen (hPL) and prolactin (PRL) have a presumed role in its pathogenesis. Aims: To assess the relationship of serum hPL and PRL with IR and β-cell function in GDM and pregnant women with normal glucose tolerance (NGT). Materials and Methods: This cross-sectional study was performed with 40 women with GDM and an equal number of pregnant women with NGT who were diagnosed on the basis of the WHO 2013 criteria during 24–40 weeks of gestation. hPL was measured by an enzyme-linked immunosorbent assay (ELISA); PRL and fasting insulin were measured by a chemiluminescent immunoassay. Equations of homeostatic model assessment (HOMA) were used to calculate the indices of IR (HOMA-IR) and β-cell function (HOMA-B). Results: No statistically significant difference was found between the GDM and NGT groups in circulating concentrations of either hPL (6.01 ± 1.76 vs. 5.92 ± 2.10 mg/L, mean ± SD; P = 0.852) or PR [180.27 (125.95–306.20) vs. 166.87 (134.24–284.70) ng/mL, median (IQR); P = 0.704]. There was no relationship of circulatory levels of hPL and PRL with glucose values at different time points during oral glucose tolerance test as well as with AUCglucose (P = NS for all). On multiple regression analysis, neither hPL nor PRL emerged as a significant predictor for fasting insulin, HOMA-IR, and HOMA-B in GDM (P = NS for all). Conclusions: Circulating concentration of hPL and PRL may not be a potential determinant of IR and β-cell dysfunction in GDM.

Keywords: GDM, HOMA-B, HOMA-IR, human placental lactogen, prolactin

How to cite this article:
Alam MF, Jahan S, Hasan M, Sultana N, Hossain M, Uddin MF, Hasanat MA. Serum human placental lactogen and prolactin may not be associated with aberrant glucose homeostasis in GDM. J Diabetol 2021;12, Suppl S1:66-72

How to cite this URL:
Alam MF, Jahan S, Hasan M, Sultana N, Hossain M, Uddin MF, Hasanat MA. Serum human placental lactogen and prolactin may not be associated with aberrant glucose homeostasis in GDM. J Diabetol [serial online] 2021 [cited 2022 Oct 6];12, Suppl S1:66-72. Available from: https://www.journalofdiabetology.org/text.asp?2021/12/5/66/321817

  Introduction Top

Pregnancy induces dynamic changes in energy metabolism along with a marked decrease in insulin sensitivity.[1] The maintenance of normal glucose homeostasis is dependent on the capability of β-cells to increase the secretion of insulin, thereby compensating for this IR.[2] An insufficient compensatory response will result in maternal hyperglycemia, as occurs in the setting of GDM.[3]

The development of the fetal–placental unit during pregnancy causes endocrine changes that trigger a shift in maternal nutrient metabolism. As pregnancy progresses and the placenta grows larger, hormone production also increases and so does the level of IR. The IR becomes apparent between 20 and 24 weeks of pregnancy and continues to rise till the 35th week when the growth of placenta stops.[4] The fact that IR rapidly abates after delivery suggests that placental hormones are the major contributor to this state.[5]

hPL is regarded as the main diabetogenic hormone synthesized from the fetal–placental unit.[1] hPL stimulates lipolysis, leading to an increase in circulating free fatty acids. It provides a different fuel for the mother so that glucose and amino acids can be conserved for the fetus. The increase in free fatty acid levels, in turn, directly interferes with insulin-directed entry of glucose into cells.[4] Therefore, hPL is considered as a potent antagonist to insulin action during pregnancy.[1]

As stated earlier, the maintenance of normal glucose homeostasis in pregnancy is dependent on the capacity of the pancreatic β-cells to increase insulin secretion.[6] Importantly, the underlying mechanisms of both normal β-cell adaptation in human pregnancy and its aberrance in GDM are not well understood.[2] The current model for islet adaptation in pregnancy is that circulating factors in maternal serum stimulate the expansion of β-cell mass.[7] In this context, animal and preclinical studies have suggested that the hormones PRL and hPL may stimulate β-cell growth, insulin secretion and promote the expression of antiapoptotic proteins.[2],[8]

During pregnancy, the peak in β-cell proliferation coincides with increased PRL and/or hPL levels.[9] In vitro studies have demonstrated that both PRL and hPL bind to the PRL receptor on the β-cell and induce a series of downstream intracellular mediators to promote its growth and proliferation.[2] This mechanism also increases insulin secretory capacity by enhancing the expression of glucose sensors, which is critical for maintaining optimal glucose homeostasis during pregnancy.[2],[10],[11],[12]

In spite of the existing hypotheses and evidence from preclinical studies, available data suggest a complex relationship between hPL, PRL, and glucose homeostasis in pregnancy. The relationship of GDM with the circulatory level of these hormones is not yet consolidated. There has been limited evaluation, and the few previous clinical studies have yielded conflicting findings.[2] Thus, our objective in the current study was to evaluate the association of hPL and PRL with IR and β-cell function in GDM.

  Materials and Methods Top

Selection of participants

The present study encompassed 40 women with GDM (age: 28.20 ± 5.00 years, BMI: 27.41 ± 3.37kg/m2; mean ± SD) and an equal number of women with NGT (age: 26.23 ± 4.64 years, BMI: 25.70 ± 3.71kg/m2; mean ± SD) who were screened by 75-g 3-samples oral glucose tolerance test (OGTT) following the WHO 2013 criteria for GDM. Women with a singleton pregnancy after 24 weeks of gestation who were attending the “GDM Clinic” of our department were screened and enrolled consecutively. Women with a prior history of diabetes mellitus (DM) and diabetes in pregnancy (DIP) were excluded from this study.

Study design

This cross-sectional study was carried out from April 2017 to September 2017. Prior to commencement of this study, the research protocol was approved by the Institutional Review Board (IRB). After recording relevant clinical data, OGTT was performed after an overnight fast. Study subjects were enrolled as GDM or NGT on the basis of the WHO 2013 diagnostic criteria. Thus, 40 patients with GDM and an equal number of mothers with NGT were enrolled for the study. Fasting venous blood (4 mL) was collected for hormonal assay from each subject during OGTT, and serum was separated to be preserved at –80oC until further assay.

Analytic method

Plasma glucose was analyzed by the glucose oxidase method by using Dimension EXL 200 Integrated Chemistry System (Siemens, Germany) on the same day of collection. Serum insulin levels were measured by the chemiluminescent immunoassay method using the Access Immunoassay System (REF- 33410), Beckman Coulter, Inc., USA. The coefficient variances (CV) for glucose were 2.02% for low-level values and 2.07% for high-level values, whereas the intra-assay CV for insulin was 2.54%.

hPL was measured by the ELISA method using DRG hPL micro-ELISA kit (EIA-1283) from DRG Instruments GmbH, Germany. Quantitative determination of serum PRL levels was done by the chemiluminescent immunoassay method using Access Immunoassay System (Cat. No. 33530), Beckman Coulter, Inc., USA. A quality control (QC) serum pool was included with mean 4.91 mg/L and CV 10.79% during the hPL assay. Pipetting of all samples and controls was completed within 3 min as per the manufacturer’s recommendation. For PRL, the QC serum pool had a mean of 6.03ng/mL and an intra-assay CV of 2.20%.

Measurement of insulin secretion and sensitivity index

IR and secretion were calculated by using the equations of the original HOMA model described by Matthews et al.[13]



Statistical analysis

All data were analyzed by using SPSS program (version 23.0). Continuous variables were tested for normality by the Shapiro–Wilk test and natural log transformation of skewed variables were used, where necessary, in subsequent analyses. Data were expressed as frequencies or percentages for qualitative values and mean (±SD) for quantitative values with normal distribution. When quantitative values with skewed distribution were found, they were presented as median and interquartile range (25th–75th percentile). The total area under curve for glucose (AUCglucose) on OGTT from 0 hour to 02 hour was calculated by using trapezoidal rule. Comparison between subgroups based on OGTT status was done by Chi-square test, unpaired t-test, or Mann–Whitney U test as applicable. The univariate association of AUCglucose with hPL and PRL, respectively, was plotted according to OGTT status and assessed by Pearson’s correlation coefficient test. Correlations of hPL and PRL with glucose profile and various insulin indices were analyzed by Pearson’s/Spearman’s correlation test as applicable. In both GDM and NGT groups, multiple linear regression analyses of the following dependent variables were done: log fasting insulin (Panel A), log HOMA-IR (Panel B), and log HOMA-B (Panel C). These models were adjusted for age, gestational weeks, BMI, and family history of diabetes. P value ≤ 0.05 was considered statistically significant.

Ethical clearance

Ethical approval for this study was provided by the Institutional Review Board of Bangabandhu Sheikh Mujib Medical University on 8 January 2017.

  Results Top

As shown in [Table 1], women with GDM were older than those in the NGT group (P = 0.071) and they had significantly higher BMI values than their peers (P = 0.034). Further, subjects with GDM were more likely to have a family history of diabetes (P = 0.098). The mean weeks of gestation at the OGTT were similar between groups (GDM vs. NGT; 31.38 ± 4.21 vs. 31.40 ± 4.71 weeks, mean ± SD). As anticipated, the GDM group exhibited higher dysglycemia (fasting, 1 hour and 2 hour plasma glucose and AUCglucose, for all P < 0.001). The GDM group had significantly higher IR, as indicated by a higher fasting insulin value (P = 0.001) and HOMA-IR (P < 0.001) and poor β-cell secretion (HOMA-B: P = 0.014). There was no statistically significant difference between the GDM and NGT groups in circulating concentrations of either hPL (6.01 ± 1.76 vs. 5.92 ± 2.10 mg/L, mean ± SD; P = 0.852) or PRL [180.27 (125.95–306.20) vs. 166.87 (134.24–284.70) ng/mL, median (IQR); P = 0.704].
Table 1: Clinical and metabolic characteristics of study subjects

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Relationship of hPL and PRL with glycemia

[Table 2] shows the correlations of hPL and PRL with glucose profile during OGTT. hPL did not correlate with PG in GDM (0h PG: P = 0.418; 01-h PG: P = 0.831; 02-h PG: P = 0.318). Similarly, there was no correlation between PRL and glucose profile in GDM (0h PG: P = 0.521; 01-h PG: P = 0.382; 02-h PG: P = 0.126).
Table 2: Correlations of hPL and PRL with glucose profile during 75 g OGTT

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[Figure 1] shows the relationships between AUCglucose on the OGTT with hPL and PRL, respectively. In both the GDM and NGT, there was no association between AUCglucose and either hPL (GDM: P = 0.712; NGT: P = 0.544) or PRL (GDM: P = 0.219; NGT: P = 0.814).
Figure 1: Plots of AUC glucose on the OGTT vs. hPL (A) and prolactin (B) in study subjects. by Pearson’s correlation coefficient test; AUC glucose = area under curve for glucose; GDM = gestational diabetes mellitus; NGT = normal glucose tolerance; OGTT = oral glucose tolerance test; hPL = human placental lactogen

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Relationship of hPL and PRL with IR and β-cell function

[Table 3] revealed the statistically significant association of hPL with fasting insulin (P = 0.040) and HOMA-IR (P = 0.022) in NGT but not in GDM (fasting insulin: P = 0.189; HOMA-IR: P = 0.258). hPL had no correlation with HOMA-B in either group (GDM: P = 0.163; NGT: P = 0.657). On the other hand, PRL had no correlation with insulin indices either in GDM (fasting insulin: P = 0.891; HOMA-IR: P = 0.747; HOMA-B: P = 0.727) or in NGT (fasting insulin: P = 0.897; HOMA-IR: P = 0.858; HOMA-B: P = 0.919).
Table 3: Correlations of hPL and PRL with various insulin indices

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Multiple linear regression of dependent variables revealed no significant association of hPL and PRL with either fasting insulin ([Figure 1A]) or HOMA-IR ([Figure 1B]) in women with both GDM and NGT (P = NS for all). Similarly, no significant association of hPL and PRL was found with HOMA-B in either group (P = NS for all) [Table 4].
Table 4: Multiple regression showing association of hPL and prolactin with dependent variables: log fasting insulin (Panel A), log HOMA-IR (Panel B), and log HOMA-B (Panel C), respectively, in women with or without GDM. All of the multiple linear regression models were adjusted for age, gestational weeks, BMI, and family history of DM

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  Discussion Top

The present study demonstrated that circulating concentrations of hPL and PRL do not differ between women with GDM and NGT. hPL had a relationship with IR in pregnant women with NGT but not in GDM. Neither hPL nor PRL was associated with β-cell function in either group of women.

GDM is a result of both pancreatic β-cell insufficiency and increased IR, in which genetic predisposition and various humeral factors might be involved.[14] Accumulative results of various preclinical in vitro investigations have suggested that placental hormones such as hPL and PRL have a definite role in the pathogenesis of GDM.[11],[15] However, observations resulting from the current study dictate that circulating concentrations of hPL and PRL do not differ between GDM and pregnancy without glucose abnormality. As stated earlier, it has been hypothesized that maternal hPL and PRL may relate to a women’s underlying glucoregulatory physiology during pregnancy and its aberrance leads to GDM. However, human data relevant to this appliance remain limited. Indeed, studies have reported similar,[16],[17],[18],[19],[20],[21],[22] higher,[23],[24],[25],[26],[27] and lower[28] serum concentrations of both hPL and PRL in GDM, as compared with their peers. Variation of results might be explained by different aspects, such as studies conducted in the past era used different diagnostic criteria; as for GDM, diagnostic criteria were not clearly established previously. There were modest sample size (ranging from 20 to 50 subjects, of whom 8 to 25 had GDM) and diverse assay methods in those studies.

A very recent study by Retnakaran et al. evaluating the relationships of these hormones to glucose homeostasis and various insulin indices in 395 pregnant women (including 105 with GDM) revealed that there is no difference in circulating levels of hPL and PRL between GDM and NGT.[2] They also concluded that circulatory levels of hPL and PRL are not associated with glucose intolerance, β-cell dysfunction, and IR in GDM. Similarly, the present study also revealed that there is no significant difference in serum hPL and PRL concentrations between women with GDM and their peers. There was no relationship of circulatory concentration of hPL and PRL with glucose values at different time points during OGTT as well as with AUCglucose. The magnitude of glucose intolerance is not equal in GDM and because of the variance in the magnitude of plasma glucose in GDM, it might not be possible to establish a linear relationship between the circulatory level of these hormones and dysglycemia. So, in contrast to previous findings that higher PRL levels might be associated with dysglycemia in pregnancy,[29] this study suggests that merely a change in the circulatory concentration of these lactogenic hormones might have no effect on glucose intolerance in GDM.

It should be noted that serum hPL and PRL were not associated with indices of IR and β-cell dysfunction in GDM and that was in agreement with the observations of the other authors.[2] Although there was a linear relationship between hPL and indices of IR in NGT, no such association was found in GDM. hPL is believed to have a role in pregnancy-induced IR, even in normoglycemic women. However, the pathophysiology of GDM is complex. Numerous factors such as placental hormones, genetic and epigenetic contributions, obesity, adipokines such as leptin and adiponectin, various cytokines, physical inactivity, and gut microbiome influence IR and secretion in GDM.[30] Moreover, recent studies also revealed the potential effect of risk factors of GDM on the secretion of placental hormones, particularly hPL. Obesity is most often associated with lower hPL concentrations, whereas pregestational diabetes results in increased hPL levels in pregnancy.[31] A significant decrease in hPL RNA levels (75%) was observed in term placentas obtained from obese women (prepregnancy BMI >35kg/m2), compared with those with normal BMI (BMI 20–25kg/m2).[32] On the other hand, adipocytokines such as leptin were found to be unable to modify the secretion of hPL in pregnancy.[32] The influence of various factors on placental secretion is obvious,[31] but the causal mechanism is still not completely elucidated. This might explain why there was no relationship between serum hPL concentration and indices of IR in the GDM group.

It should be recognized that the present study does not argue against the central role of hPL and PRL in the current model of β-cell adaptation during pregnancy, for which there exists a robust body of preclinical evidence.[2],[10],[11],[33] This has been further supported by the association of PRL receptor gene polymorphism with the risk of GDM.[2],[34] hPL is also known as a potent insulin antagonist. Therefore, the present findings indicate that, notwithstanding the role of hPL and PRL in IR and β-cell adaptation during pregnancy, the measurement of the circulating concentration of hPL and PRL may not provide insight on maternal dysglycemia and the pathogenesis of GDM if not combined with molecular and genetic studies.

The present study has certain limitations. First, it investigated the circulatory levels of only two placental hormones and was unable to take into account the effect of other factors associated with GDM. Second, apart from the HOMA model, we could not calculate other indices (such as insulin secretion-sensitivity index-2, Matsuda index, insulinogenic index etc.) for estimation of IR and β-cell dysfunction. Third, owing to the cross-sectional nature no causal inference could be drawn.

To summarize, circulating levels of hPL and PRL do not differ between women with GDM and pregnancy without glucose aberrance. Though hPL might have potential influence on IR in pregnancy, changing serum concentrations of these hormones do not exhibit a relationship with glucose homeostasis in GDM. Further studies are warranted to elucidate the impact of these factors on IR and β-cell dysfunction in the setting of GDM.


The authors would like to thank the department of Microbiology, BSMMU and DNA Solution Laboratory, Dhaka for their technical support.

Financial support and sponsorship

This work was supported by BSMMU as a research grant.

Conflicts of interest

The authors declare no conflict of interest regarding the publication of this article.

  References Top

Shalayel MHF, Noaemi MC, Ahmed SAM. Insulin resistance in the third trimester of pregnancy suffering from gestational diabetes mellitus or impaired glucose tolerance. In: Radenkovic M, editor. Gestational Diabetes. Croatia: In Tech; http://www.intechopen.com/books/gestational-diabetes/insulin-resistance-in-the-third-trimester-of-pregnancy-suffering-from-gestational-diabetes-mellitus.net/; 2011 [Last accessed4 April 2017].  Back to cited text no. 1
Retnakaran R, Ye C, Kramer CK, Connelly PW, Hanley AJ, Sermer M, et al. Evaluation of circulating determinants of beta-cell function in women with and without gestational diabetes. J Clin Endocrinol Metab 2016;101:2683-91.  Back to cited text no. 2
Ferrara A, Ehrlich SF. Strategies for diabetes prevention before and after pregnancy in women with GDM. Curr Diabetes Rev 2011;7:75-83.  Back to cited text no. 3
Palani S, Joseph NM, Tegene Y, Zacharia A, Marew T. Gestational Diabetes – a review. J Global Trends Pharmaceut Sci 2014;5:1673-83.  Back to cited text no. 4
Buchanan TA, Xiang AH. Gestational diabetes mellitus. J Clin Invest 2005;115:485-91.  Back to cited text no. 5
Angueira AR, Ludvik AE, Reddy TE, Wicksteed B, Lowe WL Jr, Layden BT. New insights into gestational glucose metabolism: Lessons learned from 21st century approaches. Diabetes 2015;64:327-34.  Back to cited text no. 6
Nalla A, Ringholm L, Søstrup B, Højrup P, Thim L, Levery SB, et al. Implications for the offspring of circulating factors involved in beta cell adaptation in pregnancy. Acta Obstet Gynecol Scand 2014;93:1181-9.  Back to cited text no. 7
Wang T, Lu J, Xu Y, Li M, Sun J, Zhang J, et al. Circulating prolactin associates with diabetes and impaired glucose regulation. Diabetic Care 2013;36:1974-80.  Back to cited text no. 8
Parsons JA, Brelje TC, Sorenson RL. Adaptation of islets of langerhans to pregnancy: Increased islet cell proliferation and insulin secretion correlates with the onset of placental lactogen secretion. Endocrinology 1992;130:1459-66.  Back to cited text no. 9
Ramos-Román MA. Prolactin and lactation as modifiers of diabetes risk in gestational diabetes. Horm Metab Res 2011;43:593-600.  Back to cited text no. 10
Xu Y, Wang X, Gao L, Zhu J, Zhang H, Shi H, et al. Prolactin-stimulated survivin induction is required for beta cell mass expansion during pregnancy in mice. Diabetologia 2015;58:2064-73.  Back to cited text no. 11
Napso T, Yong HEJ, Lopez-Tello J, Sferruzzi-Perri AN. The role of placental hormones in mediating maternal adaptations to support pregnancy and lactation. Front Physiol 2018;9:1091.  Back to cited text no. 12
Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: Insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia 1985;28:412-9.  Back to cited text no. 13
Chatterjee S. Pathogenesis of gestational diabetes mellitus. In: Seshiah V, editor. Contemporary Topics in Gestational Diabetes Mellitus. 1st ed. New Delhi: Jaypee Brothers;2015, p. 18-23.  Back to cited text no. 14
Ernst S, Demirci C, Valle S, Velazquez-Garcia S, Garcia-Ocaña A. Mechanisms in the adaptation of maternal beta-cells in pregnancy. Diabetes Management 2011;1:239-48.  Back to cited text no. 15
Park S, Kim MY, Baik SH, Woo JT, Kwon YJ, Daily JW, et al. Gestational diabetes is associated with high energy and saturated fat intakes and with low plasma visfatin and adiponectin levels independent of pre-pregnancy BMI. Eur J Clin Med 2013;67:196-201.  Back to cited text no. 16
Skouby SO, Kühl C, Hornnes PJ, Andersen AN. Prolactin and glucose tolerance in normal and gestational diabetic pregnancy. Obstet Gynecol 1986;67:17-20.  Back to cited text no. 17
Montelongo A, Lasunción MA, Pallardo LF, Herrera E. Longitudinal study of plasma lipoproteins and hormones during pregnancy in normal and diabetic women. Diabetes 1992;41:1651-9.  Back to cited text no. 18
Luthman M, Stock S, Werner S, Bremme K. Growth hormone-binding protein in plasma is inversely correlated to placental lactogen and augmented with increasing body mass index in healthy pregnant women and women with gestational diabetes mellitus. Gynecol Obstet Invest 1994;38:145-50.  Back to cited text no. 19
Milasinović L, Djurdjević J, Dokmanović-Djordjević M, Djordjević A, Petrović D, Milasinović L, et al. [Prolactin levels in pregnant women with glucose intolerance at full-term delivery]. Med Pregl 1997;50:269-73.  Back to cited text no. 20
Grigorakis SI, Alevizaki M, Beis C, Anastasiou E, Alevizaki CC, Souvatzoglou A. Hormonal parameters in gestational diabetes mellitus during the third trimester: High glucagon levels. Gynecol Obstet Invest 2000;49:106-9.  Back to cited text no. 21
Shalayel MH, Idris SA, Mohammed MS, Mohammed SA. Prolactin and insulin estimates in pregnancy with glucose intolerance. Khartoum Med J 2009;2:200-5.  Back to cited text no. 22
Kirwan JD, Larraine HP, Satish CK, Catalano PM. Clinically useful estimates of insulin sensitivity during pregnancy - Validation studies in women with normal glucose tolerance and gestational diabetes mellitus. Diabetic Care 2001;24:1602-07.  Back to cited text no. 23
Lopez-Espinoza I, Smith RF, Gillmer M, Schidlmeir A, Hockaday TD. High levels of growth hormone and human placental lactogen in pregnancy complicated by diabetes. Diabetes Res 1986;3:119-25.  Back to cited text no. 24
Handerson CE, Divon MY. Combining human placental lactogen with routine glucose challenge test. Prim Care Update Ob Gynes 1998;5:189-90.  Back to cited text no. 25
Couch SC, Philipson EH, Bendel RB, Pujda LM, Milvae RA, Lammi-Keefe CJ. Elevated lipoprotein lipids and gestational hormones in women with diet-treated gestational diabetes mellitus compared to healthy pregnant controls. J Diabetes Complications 1998;12:1-9.  Back to cited text no. 26
Sattar SA, Abdullah AH, Nsaif AS. Gestational diabetes mellitus and hormonal alteration. Iraqi J Pharm Sci 2016;25:37-41.  Back to cited text no. 27
Olszewski J, Szczurowicz A, Wójcikowski C. [Changes in levels of human placenta lactogen (hpl), progesterone, and estriol in blood serum and estrogens in urine during gestational diabetes mellitus]. Ginekol Pol 1995;66:145-50.  Back to cited text no. 28
Ekinci EI, Torkamani N, Ramchand SK, Churilov L, Sikaris KA, Lu ZX, et al. Higher maternal serum prolactin levels are associated with reduced glucose tolerance during pregnancy. J Diabetes Investig 2017;8:697-700.  Back to cited text no. 29
Kampmann U, Knorr S, Fuglsang J, Ovesen P. Determinants of maternal insulin resistance during pregnancy: An updated overview. J: Diabetes Res2019;5320156:1-9.  Back to cited text no. 30
Sibiak R, Jankowski M, Gutaj P, Mozdziak P, Kempisty B, Ożegowska EW. Placental lactogen as a marker of maternal obesity, diabetes, and fetal growth abnormalities: Current knowledge and clinical perspectives. J Clin Med 2020;9:1142.  Back to cited text no. 31
Jin Y, Vakili H, Liu SY, Menticoglou S, Bock ME, Cattini PA. Chromosomal architecture and placental expression of the human growth hormone gene family are targeted by pre-pregnancy maternal obesity. Am J Physiol Endocrinol Metab 2018;315:E435-45.  Back to cited text no. 32
Newbern D, Freemark M. Placental hormones and the control of maternal metabolism and fetal growth. Curr Opin Endocrinol Diabetes Obes 2011;18:409-16.  Back to cited text no. 33
Le TN, Elsea SH, Romero R, Chaiworapongsa T, Francis GL. Prolactin receptor gene polymorphisms are associated with gestational diabetes. Genet Test Mol Biomarkers 2013;17: 567-71.  Back to cited text no. 34


  [Figure 1]

  [Table 1], [Table 2], [Table 3], [Table 4]


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