Gestational Diabetes Mellitus: The Impact of Body Mass Index on Clinical Outcomes

Abstract

Background:

Increasing maternal body mass index (BMI) represents a risk factor for Gestational Diabetes Mellitus (GDM) and adverse obstetrical and perinatal outcomes.

Objective:

To stratify clinical outcomes for pregnancies affected by GDM according to maternal BMI.

Methods:

Retrospective cohort study including individuals ≥18 years of age who were diagnosed with GDM from 2018 to 2022. Universal GDM screening was employed with a 50 g oral glucose challenge test ± a 100 g oral glucose tolerance test. Maternal demographics, preexisting medical conditions, and selected obstetric and neonatal morbidities were evaluated.

Results:

A total of 2193 pregnancies in 2110 women affected by GDM were identified. This included 506 (23.0%) with normal baseline maternal BMI, 596 (27.2%) with overweight, and 1091 (49.7%) with obese BMI. Adverse maternal outcomes were more frequent in the obese compared to overweight or normal BMI categories (cesarean delivery: normal 26.9% vs. overweight 28.5% vs. obese 40.9%; p < 0.001; hypertensive disorders of pregnancy: normal 8.7% vs. overweight 12.1% vs. obese 16.8%; p < 0.001). Postpartum glucose intolerance was higher in women with obesity (normal 7.3% vs. overweight 5.9% vs. obese 14.9%; p < 0.001). Infants born to mothers with obesity had higher birthweights (normal 3.3 kg vs. overweight 3.4 kg vs. obese 3.5 kg; p < 0.001), were more likely to have neonatal hypoglycemia (normal 29.4% vs. overweight 24.3% vs. obese 41.9%; p < 0.001) and require intensive care unit admission (normal 8.1% vs. overweight 5.9% vs. obese 11.9%; p < 0.001).

Conclusions:

Patients with GDM and baseline BMI in the obese range experienced the highest rate of adverse outcomes, while those with overweight BMI had similar outcomes to individuals who had normal BMI at baseline.

Introduction

Gestational diabetes mellitus (GDM) affects approximately 14% of pregnancies worldwide,¹ with significant differences across race and ethnicity subgroups.² Individuals with GDM experience an increased risk of adverse pregnancy outcomes: gestational hypertension rates increase by 50% and cesarean delivery rates increase by 30%. Neonates incur a 70% increased risk of prematurity and are 30% more likely to be large for gestational age.³ Approximately 40% of infants born to women with GDM experience neonatal hypoglycemia, which frequently requires neonatal intensive care unit admission and prolonged hospitalization.⁴ There is also accumulating evidence that intrauterine exposure to maternal hyperglycemia confers a higher risk of childhood adiposity, insulin resistance, and adverse neurodevelopmental outcomes.^5

–8

Increasing maternal body mass index (BMI) is a well-established risk factor for GDM development, and BMI ≥25–30 kg/m² is often used as a criterion in risk factor-based screening programs.⁹ However, depending on the population under study, 25–70% individuals who develop GDM have a normal baseline BMI by standard criteria.^10

–13 As individuals with GDM are typically considered as a single homogenous group, existing data are unclear on whether normal maternal BMI is associated with more favorable outcomes in the context of this diagnosis, particularly in a United States-based population. Furthermore, many prior studies examining maternal weight fail to address modifications of BMI category thresholds for patients of Asian descent as a result of their different distribution of body fat, which raises the risk of multiple metabolic comorbidities at lower BMI ranges.¹⁴ On the other hand, when using oral glucose tolerance testing, individuals of lower body weight are more likely to be diagnosed with diabetes than relatively larger size individuals, raising concern for potential GDM overdiagnosis in normal weight individuals and supporting the argument for weight-adjusted oral glucose dosing.^15,16

Our aim was to evaluate clinical pregnancy outcomes according to maternal baseline BMI category in a cohort of individuals with GDM, hypothesizing that patients with normal BMI would experience lower rates of adverse pregnancy outcomes compared with overweight or obese patients.

Materials and Methods

This was a retrospective cohort study. Following approval from the Mayo Clinic Institutional Review Board, we conducted a search of the Mayo Clinic electronic medical record system using Mayo Data Explorer (MDE). MDE is a Mayo Clinic-developed data exploration and retrieval tool that facilitates searching of data from multiple clinical and hospital source systems, including Mayo Clinic’s Unified Data Platform data warehouse environment. The Unified Data Platform was created from multiple source systems to provide researchers access to Mayo Clinic—wide clinical data in a single centralized database. Data source systems include electronic and scanned medical records, including patient demographics, diagnoses, hospital and outpatient clinical notes, and laboratory data.

We conducted an initial broad search using the following criteria: all diagnoses containing “gestational diabetes” or “GDM” or AND all diagnoses containing “pregnancy” AND gender equal to “female”, “unknown” or “other” AND “age ≥18 years”. By manual review of this list, we identified individuals ≥18 years who had singleton pregnancies with GDM over a five-year period from January 1^st, 2018, and December 31^st, 2022, and received prenatal care at Mayo Clinic Rochester, Minnesota and three Mayo Clinic Health System sites (Mankato, Minnesota; Eau Claire, Wisconsin; and La Crosse Wisconsin). Patients with pregestational diabetes (diagnosed before or during pregnancy) and those who miscarried (delivery prior to 20 weeks of gestation) were excluded. In addition to crosschecking electronically retrieved data, additional demographic information and clinical variables were manually extracted directly from the electronic medical record for everyone by six physicians (M.M., S.P., N.V., K.S.R., M.T., and M.H.) following a standardized protocol with two physicians (M.M. and A.M.E.) crosschecking the abstracted data for accuracy.

GDM diagnosis and treatment

At the time of the study, the first trimester screening for preexisting diabetes was optional, with HbA1c recommended in individuals with risk factors for type 2 diabetes. The institution recommended universal GDM screening with a 1-hr 50 g glucose challenge test at 24–28 weeks of gestation. If the result is ≥190 mg/dL, the patient is diagnosed with GDM. If the result is ≥140 to 190 mg/dL, a 3-hr 100 g oral glucose tolerance test is advised. GDM is diagnosed based on ≥2 thresholds being equal to or exceeding the Carpenter and Coustan criteria for GDM.¹⁷ Following diagnosis, individuals with GDM meet with a certified diabetes care and education specialist and registered dietician who provide dietary education and nutritional recommendations. Capillary glucose monitoring is performed in both fasting and postprandial (1- or 2-hs after each meal) states, with target values of <95 mg/dL fasting, <140 mg/dL 1-hr post-prandially, or <120 mg/dL 2-hs post-prandially. Typically, if >20% values are above goal, pharmacological therapy is initiated, with insulin being the preferred choice. Exceptions to this screening approach include those with preexisting diabetes (diagnosis before pregnancy or at first-trimester screening), prior bariatric surgery, or patient request. In the latter two circumstances, serial capillary glucose monitoring as outlined below is recommended, with diagnosis of GDM assigned if >20% values are above goal over a 2-week period.

Demographic measurements

Demographic variables included age, BMI, self-identified ethnicity, parity, self-identified race, primary language, and glucose challenge test results. Pre-pregnancy BMI (within 3 months of pregnancy confirmation) was used as the baseline BMI. If unavailable, the BMI obtained at the time of initial obstetric visit was used. For individuals that self-identified as Asian, we adjusted BMI categories: <23 kg/m² for normal weight, 23–30 kg/m² for overweight, and >30 kg/m² for obese. For all other individuals, BMI categories were based on standard definitions: <25 kg/m² for normal weight, 25–30 kg/m² for overweight, and >30 kg/m² for obese.

Outcome measurements

Outcomes were selected based on a relevant core outcome set.¹⁸ Examined maternal outcomes included: hypertensive disorder of pregnancy, cesarean delivery, GDM requiring pharmacological therapy, and breastfeeding initiation during the delivery hospitalization. Chronic hypertension was defined as hypertension diagnosed or present before pregnancy or <20 weeks of gestation.¹⁹ Hypertensive disorders of pregnancy included gestational hypertension (defined as the new onset of hypertension at ≥20 weeks gestation in the absence of proteinuria or new signs of end-organ dysfunction²⁰), and preeclampsia (defined as the new onset of hypertension accompanied by proteinuria or the new onset of hypertension and significant end-organ dysfunction with or without proteinuria after 20 weeks of gestation²⁰). Follow-up maternal data were collected, including completion and results of a 6- to 12-week postpartum glucose tolerance test and diagnosis of diabetes or prediabetes on the postpartum glucose tolerance test. Prediabetes was diagnosed on the postpartum glucose test if the fasting plasma glucose was 100 to 125 mg/dL, or the 2-hr plasma glucose was 140 to 199 mg/dL. Type 2 diabetes mellitus was diagnosed on the postpartum glucose test if the fasting plasma glucose was ≥126 mg/dL or if the 2-hr plasma glucose was ≥200 mg/dL.

The following neonatal outcomes were collected: delivery <37 weeks gestation, livebirth, birthweight, Activity Pulse Grimace Appearance Respiration (APGAR) score at 1 minute, presence of a congenital anomaly, neonatal hypoglycemia, and admission to the neonatal intensive care unit (NICU). Congenital anomalies were documented if they met the criteria of the Centers for Disease Control and Prevention, including selected external and internal major congenital anomalies.²¹ Neonatal hypoglycemia was defined as a neonatal glucose level than or equal to 45 mg/dL (2.5 mmol/L) and/or administration of any treatment for hypoglycemia in the first 24 hr of life.

Statistical analysis

We categorized individuals according to normal, overweight, or obese baseline BMI category. Data were analyzed using BlueSky Statistics (Commercial Server Edition. Version 7.40). Comparisons between BMI categories were evaluated using chi-squared statistics or Fisher’s exact test (as appropriate) for categorical variables, and the Wilcoxon–Mann–Whitney test for continuous variables (as the relevant variables were not normally distributed based on histograms and Shapiro-Wilk testing). We conducted an additional analysis including only individuals who completed a 3-hr 100g OGTT and excluding those with congenital anomalies.

Results

A total of 2193 unique pregnancies in 2110 women were identified, 506 (23.0%) with normal baseline maternal BMI, 596 (27.2%) with overweight, and 1091 (49.7%) with obese BMI. Maternal demographics and GDM screening results are listed in Table 1. There was no difference in maternal age across BMI categories. While most pregnancies occurred in women of White race (79.8%, 1751/2193), there was greater representation of women who identified as Hispanic or Latino ethnicity in overweight and obese categories (normal 6.5% vs. overweight 11.2% vs. obese 11.3%, p < 0.001). Although there was no significant difference in the median glucose following the 50g oral glucose challenge test, we observe a progressive rise in fasting glucose values at the time of 3-hr oral glucose tolerance test across BMI categories (normal 84 mg/dL vs. overweight 90 mg/dL vs. obese 96 mg/dL, p < 0.001) and noted that patients with obesity had higher 1-hr (normal 190 mg/dL vs. obese 195 mg/dL, p < 0.001), but lower 2-hr (normal 174 mg/dL vs. obese 170 mg/dL, p < 0.001) and 3-hr (normal 133 mg/dL vs. obese 122 mg/dL, p < 0.001) glucose values compared to those with normal BMI.

Table 1.

Maternal Characteristics According to Maternal Baseline BMI

	Normal (n = 506)	Overweight (n = 596)	Obese (n = 1091)	P value	P value (normal-obese)	P value (normal-overweight)
Maternal age at delivery (years)	32 (28–35)	31 (28–35)	31 (28–35)	0.67	0.38	0.73
Parity	2 (1–3)	2 (1–3)	2 (1–3)	—	—	—
Baseline maternal BMI (kg/m²)	22.3 (20.70–23.38)	27.1 (26.0–28.3)	35.8 (32.3–40.2)	<0.001	<0.001	<0.001
Ethnicity
Hispanic/Latino	33 (6.5)	67 (11.2)	123 (11.3)	<0.001	0.01	<0.001
Not Hispanic/Latino	465 (91.9)	519 (87.0)	959 (87.9)
Not disclosed	8 (1.6)	10 (1.7)	9 (0.8)
Race Category
African American	17 (3.4)	31 (5.2)	54 (4.9)	<0.001	<0.001	<0.001
White	394 (77.9)	437 (73.3)	920 (84.3)
Asian	49 (9.7)	85 (14.3)	36 (3.3)
Other	34 (6.7)	36 (6.0)	68 (6.2)
Not disclosed	12 (2.4)	7 (1.2)	13 (1.2)
Glucose challenge test completed	476 (94.1)	564 (94.6)	1003 (91.8)	0.06	0.12	0.67
Glucose post 50 g challenge	166 (152–184)	167 (152–186)	166.0 (152–184)	0.73	0.53	0.45
3-hour OGTT completed	364 (71.9)	440 (73.8)	759 (69.6)	0.17	0.34	0.48
OGTT fasting glucose (mg/dL)	84 (78–92)	90 (83–96)	96 (88–102)	<0.001	<0.001	<0.001
OGTT 1-hour glucose (mg/dL)	190 (181–203)	193 (180–206)	195 (183–209)	<0.001	<0.001	0.30
OGTT 2-hour glucose (mg/dL)	174 (161–191.5)	172 (159–185.5)	170 (155–187)	0.003	<0.001	0.06
OGTT 3-hour glucose (mg/dL)	133 (108–153.3)	132 (109–150)	122 (98–145)	<0.001	<0.001	0.25
Early pregnancy HbA1c completed	180 (35.6)	264 (44.3)	755 (69.2)	<0.001	<0.001	0.003
Early pregnancy HbA1c (%)	5.1 (4.9–5.3)	5.1 (4.9–5.3)	5.3 (5.0–5.5)	<0.001	<0.001	0.23

Data are expressed as median (interquartile range) or N (%).

BMI, body mass index; OGTT, oral glucose tolerance test.

Maternal outcomes are presented in Table 2. In comparison to normal weight individuals, individuals with obesity had higher rates of hypertensive disorders of pregnancy (normal 8.7% vs. obese 16.8%, p < 0.001) and cesarean delivery (normal 26.9% vs. obese 40.9%, p < 0.001), with no significant differences between individuals in normal and overweight categories. The increasing BMI category was associated with increased need for pharmacological therapy for GDM (normal 19.4% vs. overweight 34.1% vs. obese 50.0%, p < 0.001). Across all categories, postpartum glucose testing (either fasting glucose, 2-hr glucose, or both) was completed following 41.0% (900/2193) pregnancies. Median fasting glucose postpartum increased with increasing BMI category (normal 89 mg/dL v overweight 92 mg/dL vs. obese 95 mg/dL, p < 0.001). Women with an obese BMI at baseline had higher rates of glucose intolerance diagnosed postpartum compared to those with normal BMI (24.8% vs. 41.3%, p < 0.001). Although breastfeeding initiation at the time of delivery hospitalization was high at >90% in all categories, there was a significant decrease in women with obese versus normal baseline BMI (normal 94.1% vs. obese 89.6%, p < 0.001).

Table 2.

Maternal Outcomes According to Maternal Baseline BMI

	Normal (n = 506)	Overweight (n = 596)	Obese (n = 1091)	P	P (normal-obese)	P (normal-overweight)
Hypertensive disorder of pregnancy	44 (8.7)	72 (12.1)	183 (16.8)	<0.001	<0.001	0.07
Hypertension before pregnancy	6 (1.2)	5 (0.8)	27 (2.5)	0.03	0.09	0.56
Aspirin use during pregnancy	76 (15.0)	107 (18.0)	334 (30.6)	<0.001	<0.001	0.19
Cesarean Delivery	136 (26.9)	170 (28.5)	446 (40.9)	<0.001	<0.001	0.54
GDM requiring pharmacological therapy	98 (19.4)	203 (34.1)	545 (50.0)	<0.001	<0.001	<0.001
Breastfeeding Initiated	476 (94.1)	561 (94.1)	977 (89.6)	<0.001	0.003	0.97
Completed postpartum fasting glucose N (%)	246 (48.6)	246 (41.3)	406 (37.2)	<0.001	<0.001	0.02
Postpartum Fasting Glucose (mg/dL)	89 (84–95)	92 (87–97)	95 (89–102)	<0.001	<0.001	<0.001
Completed 2-hr 75 g OGTT postpartum N (%)	246 (48.6)	233 (39.1)	396 (36.3)	<0.001	<0.001	0.001
Postpartum 2-hr Glucose (mg/dL)	104 (86–124.5)	102 (88–125)	110.5 (92–130)	0.01	0.006	0.69
Abnormal fasting or 2-hr postpartum glucose N (%)	n ^a = 246	n = 247	n = 407
					<0.001	0.63
	61 (24.8)	66 (26.7)	168 (41.3)	<0.001

Data are expressed as median (interquartile range) or N (%).

Denominator for this variable is anyone who had a fasting and/or a 2-hour postpartum glucose completed.

BMI, body mass index; OGTT, oral glucose tolerance test.

Neonatal outcomes are presented in Table 3. There were similar rates of livebirths and premature deliveries across BMI categories. Compared to normal weight individuals, offspring of those with obesity had a higher median birthweight (normal 3.3 kg vs. obese 3.5 kg, p < 0.001), and the frequency of macrosomia increased across all BMI categories (normal 6.9% vs. 8.4% vs. 12.6%, p < 0.001). Offspring of women with obesity had higher rates of neonatal hypoglycemia requiring treatment (normal 29.4% vs. obese 41.9%; p < 0.001), and NICU admission (normal 8.1% vs. obese 11.9%; p < 0.001) compared to those born to mothers with normal baseline BMI.

Table 3.

Neonatal Outcomes According to Maternal Baseline BMI

	Normal (n = 506)	Overweight (n = 596)	Obese (n = 1091)	P	P (normal-obese)	P (normal-overweight)
Delivery <37 weeks gestation	34 (6.7)	43 (7.2)	102 (9.3)	0.12	0.08	0.75
Livebirth	506 (100.0)	596 (100.0)	1090 (99.9)	0.60	0.49	—
Birthweight (Kg)	3.3 (3.0–3.6)	3.4 (3.0–3.6)	3.5 (3.1–3.8)	<0.001	<0.001	0.25
Macrosomia (>4 kg)	35 (6.9)	50 (8.4)	137 (12.6)	<0.001	<0.001	0.36
Apgar 1 min	8.0 (8.0–9.0)	8.0 (8.0–9.0)	8.0 (7.0–9.0)	<0.001	<0.001	0.20
Congenital Anomaly	7 (1.4)	3 (0.5)	16 (1.5)	<0.001	0.90	0.13
Neonatal hypoglycemia	149 (29.4)	145 (24.3)	457 (41.9)	<0.001	<0.001	0.06
NICU admission	41 (8.1)	35 (5.9)	130 (11.9)	<0.001	0.02	0.15
Primary reason for NICU	n = 41	n = 35	n = 130
Respiratory distress	8 (19.5)	3 (8.6)	26 (20.0)
Respiratory failure	3 (7.3)	1 (2.9)	8 (6.2)
Premature	12 (29.3)	13 (37.1)	31 (23.8)
Hypoglycemia	4 (9.8)	8 (22.9)	20 (15.4)
Other	9 (21.9)	10 (28.6)	41 (31.5)
Trisomy 21	2 (4.8)	0	1 (0.8)
Not available	3 (7.3)	0	3 (2.3)

Data are expressed as median (interquartile range) or N (%).

NICU, Neonatal Intensive Care Unit.

Our additional analyses, including only individuals who completed a 3-hr 100g OGTT (Supplementary Tables S1, S2, and S3) and excluding those with congenital anomalies (Supplementary Tables S4, S5, and S6), did not reveal any significant differences in key findings.

Discussion

When categorizing individuals with GDM according to baseline maternal BMI, we found that individuals with obesity experienced the highest frequencies of adverse clinical outcomes, while overweight and normal weight individuals experienced similar rates of adverse pregnancy outcomes. In fact, normal weight individuals experienced similar incidences of hypertensive disorders of pregnancy and cesarean delivery as their overweight counterparts, along with a comparable incidence of postpartum glucose intolerance, and their infants have similar rates of neonatal hypoglycemia and NICU admission. These findings support efforts to develop and evaluate interventions specifically for women with GDM and obesity to improve clinical outcomes.

Increasing maternal BMI is an independent risk factor for adverse pregnancy outcomes. In a similar, predominantly non-Hispanic, White population without GDM, investigators identified a BMI threshold of 28 kg/m² as being associated with a significant risk of several adverse outcomes, including cesarean delivery, preeclampsia, and increased birthweight.²² Concurrently, higher maternal BMI is a risk factor for GDM development, and our data demonstrate that even with concurrent GDM diagnosis and treatment, the presence of maternal obesity further increases maternal and infant risk. These findings are somewhat consistent with prior authors reporting that the effect of GDM decreased after adjusting for several factors, which included pre-pregnancy BMI.^12,23 Notably, we did not find differences between normal and overweight categories in terms of risk across a spectrum of maternal and infant outcomes. This finding may reflect the positive impact of treatment or heterogeneity in GDM phenotypes. In fact, Powe et al. identified a greater risk of GDM-associated adverse outcomes in women whose hyperglycemia is predominantly related to defects in insulin sensitivity, and such individuals also have higher BMI and fasting glucose compared to those with predominantly insulin secretion defects.²⁴ Similarly, we observed a progressive rise in fasting glucose across higher BMI categories, and a higher 1-hr glucose in women with obese versus normal baseline BMI. This is consistent with prior data identifying the 1-hr plasma glucose as a marker of insulin resistance and β-cell dysfunction in individuals without diabetes.²⁵ Pharmacological therapy was required in approximately 50% of pregnancies with maternal obesity, and 19% and 34% of pregnancies with normal and overweight maternal BMI, respectively. Although in the current study, home capillary glucose testing results were used as the basis for pharmacological therapy, longitudinal continuous glucose monitoring data may provide improved insights into patterns of maternal hyperglycemia associated with GDM-related adverse outcomes.²⁶

Overall, our rates of attendance at postpartum glucose tolerance testing were low; despite an electronic medical record system with automated appointment reminders and the ability for users to self-schedule appointment times, fewer than half of all testing was completed. Unfortunately, these findings are consistent with prior studies in this field,²⁷ and future efforts will focus on increasing attendance at our institution. Consideration will also be given to completing postpartum glucose tolerance testing during the delivery hospitalization, an approach which has shown to have similar diagnostic value and almost universal adherence.²⁸ This is an important issue to address, noting the overall rate of postpartum glucose intolerance of 11%; identifying these individuals can facilitate lifestyle interventions with or without metformin therapy to reduce their long-term risk of Type 2 diabetes.²⁹ Indeed, future work should also focus on determining the precise factors leading to progressive postpartum glucose intolerance in women with GDM, particularly noting the variability we observed across BMI categories.

Although our study is limited by its retrospective nature and reliance on data collected during routine clinical practice, we present detailed patient-level information with <5% missing data overall. Our obstetric practice serves predominantly our local population, which is predominantly White, non-Hispanic individuals. This is reflected in our study demographics and could limit the generalizability of our findings. However, we did adjust our BMI thresholds to ensure that individuals who identified as Asian ethnicity were appropriately categorized. Specific information was not available regarding gestational weight gain or adverse outcomes in antecedent pregnancies, factors which could modify individual risk within our cohort. As first-trimester screening for pregestational diabetes was not universal at Mayo Clinic, and attendance at postpartum testing was poor, it is possible that some of the included cases reflected pregestational diabetes, which was misdiagnosed as GDM. Since the study was completed, our institution has recommended universal screening in the first trimester for pregestational diabetes with HbA1c. Finally, we acknowledge that while diagnosing GDM based on a 1-hr glucose challenge test (≥190 mg/dL) or using capillary glucose monitoring is frequently used in real-world clinical practice, it is not a validated approach. However, we did conduct a subanalysis on individuals who completed a 3-hr OGTT and did not find any significant differences in our overall findings (see Supplementary Tables S1, S2, and S3).

Conclusions

Clinical outcomes for patients with GDM appear to correspond to baseline BMI category. Individuals with an obese BMI incur the highest risk of adverse pregnancy outcomes, whereas those with normal and overweight BMI experience similar risk.

Footnotes

Authors’ Contributions

M.M. and S.P. collected, organized, and analyzed data and drafted the article. N.V., K.S.R., M.T., and M.H. collected data. A.V. and C.H.R. analyzed and interpreted data. A.M.E. analyzed and interpreted data, supervised the study, and took final responsibility for the data presented. All authors critically reviewed and approved the article.

Data Availability Statement

Some or all data sets generated during and/or analyzed during the present study are not publicly available but are available from the corresponding author on reasonable request.

Author Disclosure Statement

The authors have no relevant disclosures or conflicts of interest.

Funding Information

A.M.E. is supported by the National Institutes of Health (award DK134767 and DK092721) and the Robert and Elizabeth Strickland Career Development Award in Endocrinology, Metabolism, Diabetes, and Nutrition. A.V. is supported by the National Institutes of Health (awards DK78646, DK116231, and DK126206).

Supplementary Material

Supplementary Tables

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