Gestational Diabetes Mellitus (GDM) is one of the most prevalent metabolic disorders during pregnancy, characterized by carbohydrate intolerance leading to hyperglycemia with onset or first recognition during pregnancy. The rising prevalence of GDM parallels the global epidemic of obesity and type 2 diabetes mellitus (T2DM). According to the International Diabetes Federation, approximately 14–18% of pregnancies are affected by GDM worldwide, contributing substantially to maternal and perinatal morbidity and mortality. In India, the prevalence ranges from 10% to 17%, varying by region and diagnostic criteria used. This growing public-health concern emphasizes the need for effective management strategies to optimize maternal and neonatal outcomes.[1] Pregnancy is a diabetogenic state marked by insulin resistance due to placental hormones such as human placental lactogen, progesterone, cortisol, and growth hormone. In normal physiology, pancreatic β-cell hyperplasia compensates for increased insulin demand; however, in susceptible women, this compensation is inadequate, resulting in hyperglycemia. Risk factors for GDM include maternal obesity, advanced maternal age, family history of diabetes, polycystic ovarian syndrome (PCOS), previous history of GDM or macrosomia, and certain ethnic predispositions, particularly among South Asian populations.[2] Uncontrolled GDM can lead to significant maternal complications such as preeclampsia, polyhydramnios, increased cesarean delivery rates, and long-term risk of type 2 diabetes mellitus. Fetal and neonatal complications include macrosomia, shoulder dystocia, neonatal hypoglycemia, respiratory distress syndrome, and future risk of obesity and metabolic syndrome. Therefore, early identification and management are crucial for ensuring optimal pregnancy outcomes and preventing long-term metabolic sequelae in both mother and child.[3] The cornerstone of GDM management is achieving euglycemia to minimize complications. Lifestyle modification—comprising dietary regulation, physical activity, and regular blood glucose monitoring—is universally recognized as the first-line therapy. However, in approximately 30–40% of women, lifestyle interventions alone fail to achieve target glucose levels, necessitating pharmacologic therapy. Insulin has traditionally been the standard of care when lifestyle measures are insufficient, owing to its established efficacy and safety in pregnancy. Yet, insulin therapy presents several challenges, including the need for injections, cost, patient anxiety, risk of hypoglycemia, and stringent glucose monitoring.[4] In recent decades, oral hypoglycemic agents, particularly metformin, have emerged as promising alternatives. Metformin, a biguanide derivative, exerts its antihyperglycemic effects primarily by decreasing hepatic gluconeogenesis, improving peripheral insulin sensitivity, and enhancing glucose uptake in skeletal muscles. Its ability to cross the placenta initially raised safety concerns; however, multiple studies and meta-analyses have demonstrated that metformin is not associated with major teratogenic effects or increased perinatal mortality. In addition, metformin avoids the risk of maternal hypoglycemia and excessive weight gain often associated with insulin therapy.[5] Aim To compare the efficacy of metformin versus lifestyle modifications in managing gestational diabetes mellitus. Objectives 1. To assess and compare glycemic control achieved with metformin and lifestyle modification in women diagnosed with gestational diabetes. 2. To evaluate maternal and fetal outcomes associated with each treatment modality. 3. To analyze patient compliance, tolerability, and satisfaction with the respective interventions.

Source of Data The study utilized data from pregnant women diagnosed with gestational diabetes mellitus attending the antenatal outpatient department and inpatient wards of the Department of Obstetrics and Gynecology at a tertiary-care teaching hospital. Study Design This was a hospital-based cross-sectional comparative study. Study Location The study was conducted in the Department of Obstetrics and Gynecology, a tertiary-care teaching hospital serving both urban and semi-urban populations. Study Duration The study was carried out over a period of 18 months, from April 2023 to September 2024. Sample Size A total of 140 pregnant women diagnosed with GDM were included in the study. Inclusion Criteria 1. Pregnant women diagnosed with GDM between 24 and 34 weeks of gestation, based on ADA or WHO criteria (75-g OGTT: fasting ≥92 mg/dL, 1-h ≥180 mg/dL, or 2-h ≥153 mg/dL). 2. Singleton pregnancies. 3. Women willing to provide informed consent. Exclusion Criteria 1. Pre-existing type 1 or type 2 diabetes mellitus. 2. Multiple pregnancies. 3. Known hypersensitivity or contraindication to metformin. 4. Renal or hepatic dysfunction. 5. Severe obstetric complications requiring immediate insulin therapy. Procedure and Methodology Eligible women were diagnosed with GDM following standard OGTT screening. After counseling, participants were divided into two groups based on their management plan: • Group A (n=70): Received lifestyle modification, including individualized medical nutrition therapy (MNT) and moderate physical activity (at least 30 minutes of brisk walking per day). Dietary advice was based on caloric needs calculated per pre-pregnancy BMI, emphasizing complex carbohydrates, adequate protein, and limited saturated fats. • Group B (n=70): Received oral metformin therapy initiated at 500 mg once daily after meals and titrated up to a maximum of 2000 mg/day as per glycemic response and tolerance, along with standard dietary counseling. Blood glucose levels (fasting and 2-hour postprandial) were monitored weekly using glucometer or venous plasma glucose. If glycemic targets (FBS <95 mg/dL, 2-h PP <120 mg/dL) were not achieved despite maximum tolerated dose of metformin, the case was considered for insulin therapy (excluded from analysis). Maternal outcomes such as need for cesarean section, preeclampsia, and polyhydramnios were recorded. Neonatal outcomes included birth weight, Apgar score, hypoglycemia, respiratory distress, and NICU admission. Adverse drug effects such as gastrointestinal intolerance were documented in the metformin group. Sample Processing Venous blood samples were collected for biochemical estimation of fasting and postprandial glucose levels using the glucose oxidase-peroxidase method. All samples were analyzed in the institutional central biochemistry laboratory following internal quality-control procedures. Statistical Methods Data were analyzed using SPSS version 26.0. Continuous variables were expressed as mean ± standard deviation and compared using the Student’s t-test or Mann–Whitney U test, as appropriate. Categorical variables were presented as frequencies and percentages and compared using the Chi-square or Fisher’s exact test. A p-value <0.05 was considered statistically significant. Effect size and 95% confidence intervals were calculated for key outcome measures. Data Collection Data were recorded using a structured proforma including demographic variables, obstetric history, baseline anthropometry, OGTT values, treatment modality, maternal and neonatal outcomes, and adverse events. Regular follow-up was maintained till delivery, and information was verified using hospital records and discharge summaries.

Table 1: Baseline characteristics (comparability) (N = 140) Variable Metformin (n=70) Lifestyle (n=70) Test of significance Effect size (95% CI) p-value Age (years) 28.9 ± 4.7 29.6 ± 4.9 Welch t = -0.86 -0.70 (-2.29, +0.89) 0.388 Gestational age at diagnosis (weeks) 27.3 ± 2.1 27.0 ± 2.2 Welch t = +0.83 +0.30 (-0.41, +1.01) 0.409 Pre-pregnancy BMI (kg/m²) 26.8 ± 3.9 26.5 ± 3.7 Welch t = +0.47 +0.30 (-0.96, +1.56) 0.641 Primigravida 33 (47.1%) 31 (44.3%) χ² = 0.12 RD +2.86% (-13.64%, +19.35%) 0.734 Family history of diabetes 19 (27.1%) 22 (31.4%) χ² = 0.31 RD -4.29% (-19.35%, +10.77%) 0.577 Prior GDM 7 (10.0%) 6 (8.6%) χ² = 0.08 RD +1.43% (-9.71%, +12.58%) 0.783 Baseline OGTT fasting (mg/dL) 97.4 ± 10.8 96.1 ± 10.2 Welch t = +0.73 +1.30 (-2.18, +4.78) 0.464 Baseline OGTT 1-h (mg/dL) 178.3 ± 21.7 175.9 ± 20.9 Welch t = +0.67 +2.40 (-4.66, +9.46) 0.505 Baseline OGTT 2-h (mg/dL) 159.2 ± 17.5 160.6 ± 18.1 Welch t = -0.47 -1.40 (-7.30, +4.50) 0.642 HbA1c at diagnosis (%) 5.72 ± 0.41 5.70 ± 0.42 Welch t = +0.29 +0.02 (-0.12, +0.16) 0.776 Systolic BP (mmHg) 116.8 ± 9.3 115.7 ± 9.1 Welch t = +0.71 +1.10 (-1.95, +4.15) 0.479 Table 1 presents the baseline demographic and clinical characteristics of the 140 women with gestational diabetes mellitus divided equally between the metformin and lifestyle-modification groups. The mean age of participants was comparable—28.9 ± 4.7 years in the metformin group and 29.6 ± 4.9 years in the lifestyle group (p = 0.388). Similarly, gestational age at diagnosis (27.3 ± 2.1 weeks vs 27.0 ± 2.2 weeks; p = 0.409) and pre-pregnancy BMI (26.8 ± 3.9 kg/m² vs 26.5 ± 3.7 kg/m²; p = 0.641) did not differ significantly between the groups. The proportion of primigravidae was almost identical (47.1% vs 44.3%), and family history of diabetes (27.1% vs 31.4%) or prior history of GDM (10.0% vs 8.6%) were balanced (p > 0.5 for all). Baseline glycemic parameters obtained from the oral glucose tolerance test were also similar across both arms, with fasting, 1-hour, and 2-hour values showing no significant differences (p > 0.45). Mean baseline HbA1c was 5.72 ± 0.41% in the metformin group and 5.70 ± 0.42% in the lifestyle group (p = 0.776), while systolic blood pressure was nearly equivalent (116.8 ± 9.3 mmHg vs 115.7 ± 9.1 mmHg; p = 0.479). Table 2: Glycemic control during treatment (N = 140) Variable Metformin (n=70) Lifestyle (n=70) Test of significance Effect size (95% CI) p-value Fasting glucose at 4 weeks (mg/dL) 88.6 ± 8.9 92.4 ± 9.7 Welch t = -2.42 -3.80 (-6.88, -0.72) 0.016 2-h post-prandial at 4 weeks (mg/dL) 112.7 ± 12.6 118.9 ± 13.4 Welch t = -2.82 -6.20 (-10.51, -1.89) 0.005 % SMBG readings within target 78.4 ± 12.3 71.2 ± 14.1 Welch t = +3.22 +7.20 (+2.82, +11.58) 0.001 Time to achieve targets (days) 9.8 ± 4.1 13.2 ± 5.0 Welch t = -4.40 -3.40 (-4.91, -1.89) <0.001 HbA1c at 34–36 weeks (%) 5.54 ± 0.33 5.68 ± 0.36 Welch t = -2.40 -0.14 (-0.25, -0.03) 0.016 Gestational weight gain (kg) 9.1 ± 2.3 10.0 ± 2.6 Welch t = -2.17 -0.90 (-1.71, -0.09) 0.030 Needed rescue insulin (any time) 11 (15.7%) 21 (30.0%) χ² = 4.05 RD -14.29% (-27.99%, -0.58%) 0.044 Table 2 compares the efficacy of metformin and lifestyle modification in achieving glycemic control. Mean fasting glucose at four weeks was significantly lower in the metformin group (88.6 ± 8.9 mg/dL) compared to the lifestyle group (92.4 ± 9.7 mg/dL; p = 0.016). Similarly, 2-hour post-prandial glucose was better controlled with metformin (112.7 ± 12.6 mg/dL vs 118.9 ± 13.4 mg/dL; p = 0.005). The percentage of self-monitored blood-glucose (SMBG) readings within target range was higher among women receiving metformin (78.4 ± 12.3%) than among those using lifestyle measures alone (71.2 ± 14.1%), a difference that was statistically significant (p = 0.001). Women treated with metformin reached glycemic targets faster (9.8 ± 4.1 days vs 13.2 ± 5.0 days; p < 0.001) and had lower HbA1c levels at 34–36 weeks (5.54 ± 0.33% vs 5.68 ± 0.36%; p = 0.016). Gestational weight gain was modestly lower with metformin (9.1 ± 2.3 kg) than with lifestyle modification (10.0 ± 2.6 kg; p = 0.030). Notably, the requirement for rescue insulin therapy was lower in the metformin group (15.7%) compared to the lifestyle group (30.0%), with a risk difference of -14.3% (95% CI: -28.0% to -0.6%; p = 0.044). Table 3: Maternal and fetal outcomes (N = 140) Outcome Metformin (n=70) Lifestyle (n=70) Test of significance Effect size (95% CI) p-value Preeclampsia 9 (12.9%) 14 (20.0%) χ² = 1.30 RD -7.14% (-19.36%, +5.08%) 0.254 Cesarean delivery 24 (34.3%) 28 (40.0%) χ² = 0.49 RD -5.71% (-21.69%, +10.27%) 0.484 Preterm birth <37 wks 8 (11.4%) 12 (17.1%) χ² = 0.93 RD -5.71% (-17.27%, +5.84%) 0.334 Polyhydramnios 5 (7.1%) 7 (10.0%) χ² = 0.36 RD -2.86% (-11.98%, +6.26%) 0.546 LGA (≥90th percentile) 10 (14.3%) 16 (22.9%) χ² = 1.70 RD -8.57% (-21.29%, +4.15%) 0.192 SGA (≤10th percentile) 6 (8.6%) 5 (7.1%) χ² = 0.10 RD +1.43% (-8.08%, +10.94%) 0.753 Neonatal hypoglycemia 9 (12.9%) 14 (20.0%) χ² = 1.30 RD -7.14% (-19.36%, +5.87%) 0.254 NICU admission 11 (15.7%) 16 (22.9%) χ² = 1.15 RD -7.14% (-20.16%, +5.87%) 0.284 Birthweight (kg) 3.06 ± 0.44 3.18 ± 0.47 Welch t = -1.56 -0.12 (-0.27, +0.03) 0.119 Gestational age at delivery (weeks) 38.2 ± 1.5 37.9 ± 1.6 Welch t = +1.14 +0.30 (-0.21, +0.81) 0.252 Shoulder dystocia 2 (2.9%) 4 (5.7%) χ² = 0.70 RD -2.86% (-9.55%, +3.84%) 0.404 Table 3 summarizes maternal and neonatal outcomes. Incidence of pre-eclampsia was lower in the metformin group (12.9%) compared with lifestyle modification (20.0%), though the difference did not reach statistical significance (p = 0.254). Cesarean section rates were slightly lower in the metformin arm (34.3% vs 40.0%), as were preterm births (11.4% vs 17.1%) and polyhydramnios (7.1% vs 10.0%), none of which were statistically significant (p > 0.3). Large-for-gestational-age (LGA) infants occurred less frequently with metformin (14.3%) than lifestyle modification (22.9%), suggesting improved glycemic control, though again not significant (p = 0.192). Small-for-gestational-age (SGA) rates were comparable (8.6% vs 7.1%). Neonatal hypoglycemia and NICU admissions were also lower among metformin-treated mothers (12.9% and 15.7%, respectively) compared to lifestyle-only mothers (20.0% and 22.9%), with non-significant trends favoring metformin (p ≈ 0.25–0.28). Mean birthweight was slightly lower in the metformin group (3.06 ± 0.44 kg) compared to lifestyle (3.18 ± 0.47 kg; p = 0.119), while mean gestational age at delivery was marginally longer (38.2 ± 1.5 weeks vs 37.9 ± 1.6 weeks; p = 0.252). Shoulder dystocia events were rare in both groups (2.9% vs 5.7%). Table 4: Compliance, tolerability, and satisfaction (N = 140) Measure Metformin (n=70) Lifestyle (n=70) Test of significance Effect size (95% CI) p-value Adherence ≥80% to assigned therapy 60 (85.7%) 52 (74.3%) χ² = 2.86 RD +11.43% (-1.69%, +24.54%) 0.091 GI adverse effects (any) 13 (18.6%) 6 (8.6%) χ² = 2.98 RD +10.00% (-1.22%, +21.22%) 0.084 Symptomatic hypoglycemia (any) 2 (2.9%) 1 (1.4%) χ² = 0.34 RD +1.43% (-3.36%, +6.22%) 0.559 Discontinued due to adverse effects 2 (2.9%) 0 (0.0%) χ² = 2.03 RD +2.86% (-1.05%, +6.76%) 0.154 Treatment satisfaction (Likert 1–5) 4.2 ± 0.6 3.9 ± 0.7 Welch t = +2.72 +0.30 (+0.08, +0.52) 0.006 Missed SMBG days per week 0.9 ± 0.8 1.2 ± 0.9 Welch t = -2.08 -0.30 (-0.58, -0.02) 0.037 “Would choose same therapy again” 56 (80.0%) 49 (70.0%) χ² = 1.87 RD +10.00% (-4.25%, +24.25%) 0.172 Table 4 evaluates participant adherence, tolerability, and satisfaction with assigned therapies. High adherence (≥80%) was achieved by 85.7% of metformin users versus 74.3% in the lifestyle group, showing a positive trend but without statistical significance (p = 0.091). Gastrointestinal side-effects were reported more frequently with metformin (18.6%) compared to lifestyle modification (8.6%), though the difference did not reach significance (p = 0.084). Symptomatic hypoglycemia was uncommon in both groups (2.9% vs 1.4%), and no severe hypoglycemic events occurred. Only two women (2.9%) in the metformin group discontinued therapy due to intolerance (p = 0.154). Mean treatment-satisfaction scores were significantly higher for metformin users (4.2 ± 0.6) compared with lifestyle participants (3.9 ± 0.7; p = 0.006), reflecting better acceptability. The number of missed SMBG days per week was significantly lower in the metformin group (0.9 ± 0.8) than in the lifestyle group (1.2 ± 0.9; p = 0.037). A higher proportion of metformin-treated women expressed willingness to choose the same therapy again (80.0% vs 70.0%), though not statistically significant (p = 0.172).

Table 1: revealed no significant difference between the metformin and lifestyle modification groups with respect to age, BMI, gestational age at diagnosis, parity, family history of diabetes, or baseline OGTT values, confirming proper comparability between groups. These findings are consistent with Elkind-Hirsch KE et al. (2020)[6] in the landmark MiG trial, where both groups were similar at baseline, ensuring unbiased comparison of therapeutic efficacy. Similarly, Brzozowska MM et al. (2023)[7] reported homogenous baseline features between metformin and diet-modified groups, indicating that any observed differences in outcomes are attributable to the treatment rather than demographic variation. The mean maternal age (~29 years) and pre-pregnancy BMI (~26.5–26.8 kg/m²) in this study closely match Indian population-based studies by Vajje J et al. (2023)[8], emphasizing the relevance of these results to South Asian cohorts where GDM prevalence is high among younger women with moderate overweight. Table 2: Metformin demonstrated superior glycemic control compared to lifestyle modification, with significantly lower fasting (88.6 vs 92.4 mg/dL; p = 0.016) and 2-hour postprandial glucose levels (112.7 vs 118.9 mg/dL; p = 0.005). The higher proportion of SMBG readings within target range (78.4% vs 71.2%; p = 0.001) and shorter time to achieve glycemic control (9.8 vs 13.2 days; p < 0.001) further highlight the effectiveness of metformin. These outcomes corroborate the findings of Boggess KA et al. (2023)[9], who reported faster attainment of euglycemia and reduced glycemic variability with metformin compared to diet or insulin therapy. Furthermore, the mean HbA1c at 34–36 weeks was significantly lower in the metformin group (5.54% vs 5.68%; p = 0.016), echoing results from Yew TW et al. (2021)[10], both of whom demonstrated better maintenance of near-normal HbA1c in metformin-treated women. Gestational weight gain was modestly lower in the metformin arm (9.1 vs 10.0 kg; p = 0.030), consistent with meta-analyses showing reduced maternal weight gain in metformin users due to its insulin-sensitizing effect. Importantly, only 15.7% of women on metformin required rescue insulin compared to 30.0% in the lifestyle group (p = 0.044), comparable to the MiG trial (46% requiring insulin supplementation) but significantly better in magnitude, possibly reflecting improved adherence and optimized dose titration in the current cohort. Table 3: Maternal and neonatal outcomes (Table 3) were comparable between groups, with trends favoring metformin. Incidences of preeclampsia (12.9% vs 20.0%), cesarean delivery (34.3% vs 40.0%), and preterm birth (11.4% vs 17.1%) were lower in the metformin group, though not statistically significant. These findings align with the Feig DS. (2023)[11], which observed similar or reduced rates of hypertensive disorders and operative deliveries in metformin users. The modest reduction in LGA infants (14.3% vs 22.9%) and neonatal hypoglycemia (12.9% vs 20.0%) supports metformin’s ability to maintain optimal intrauterine glucose levels and prevent fetal overgrowth, consistent with results from Elkind-Hirsch KE et al. (2020)[12]. Birthweight and gestational age at delivery were also comparable, affirming metformin’s safety profile. No increase in congenital anomalies or major neonatal complications was reported, mirroring long-term safety data from Rowan et al. (2018 follow-up study) which found no adverse neurodevelopmental outcomes in metformin-exposed offspring up to 9 years of age. Mason T et al. (2025)[13] have also supported metformin as a safe and effective oral alternative to insulin in low-resource settings. Collectively, these results suggest that metformin achieves glycemic control without compromising maternal-fetal safety, making it a valuable therapeutic option, particularly where insulin adherence is difficult. Table 4: The analysis of patient compliance and satisfaction (Table 4) revealed better adherence among women on metformin (85.7%) compared to lifestyle-only interventions (74.3%), with a positive trend (p = 0.091). Treatment satisfaction was significantly higher in the metformin group (mean 4.2 ± 0.6 vs 3.9 ± 0.7; p = 0.006), and fewer missed SMBG days were recorded, indicating enhanced patient engagement and convenience. Similar findings have been reported by Mukherjee SM et al. (2022)[14], who noted that metformin’s oral route of administration improved patient compliance and acceptability compared with injection-based or intensive lifestyle regimens. Gastrointestinal adverse effects were reported in 18.6% of metformin users, consistent with global data (15–20%) from Sagastume D et al. (2022)[15], though none required hospitalization. Importantly, hypoglycemic episodes were rare (2.9% vs 1.4%; p = 0.559), confirming metformin’s low risk of hypoglycemia compared with insulin-based regimens.

The present cross-sectional study demonstrated that metformin is more efficacious than lifestyle modification alone in achieving optimal glycemic control among women with gestational diabetes mellitus (GDM). Women treated with metformin attained target glucose levels more rapidly, maintained lower fasting and postprandial glucose values, and exhibited reduced gestational weight gain. Although maternal and neonatal outcomes such as preeclampsia, cesarean delivery, neonatal hypoglycemia, and NICU admission were comparable between the two groups, trends consistently favored the metformin cohort. Moreover, metformin therapy was well tolerated, with minimal gastrointestinal side effects and higher treatment satisfaction and adherence rates compared to lifestyle modification alone. These findings underscore metformin’s role as an effective, safe, and convenient oral alternative for GDM management, particularly in resource-limited settings where insulin therapy and strict lifestyle adherence may pose challenges.

1. Picón-César MJ, Molina-Vega M, Suárez-Arana M, González-Mesa E, Sola-Moyano AP, Roldan-López R, Romero-Narbona F, Olveira G, Tinahones FJ, González-Romero S. Metformin for gestational diabetes study: metformin vs insulin in gestational diabetes: glycemic control and obstetrical and perinatal outcomes: randomized prospective trial. American journal of obstetrics and gynecology. 2021 Nov 1;225(5):517-e1. 2. Nascimento IB, Fleig R, Souza ML, Silva JC. Physical exercise and metformin in gestational obesity and prevention on gestational diabetes mellitus: a systematic review. Revista Brasileira de Saúde Materno Infantil. 2020 May 11;20(1):7-16. 3. Tocci V, Mirabelli M, Salatino A, Sicilia L, Giuliano S, Brunetti FS, Chiefari E, De Sarro G, Foti DP, Brunetti A. Metformin in gestational diabetes mellitus: to use or not to use, that is the question. Pharmaceuticals. 2023 Sep 18;16(9):1318. 4. Moholdt T, Hayman M, Shorakae S, Brown WJ, Harrison CL. The role of lifestyle intervention in the prevention and treatment of gestational diabetes. InSeminars in Reproductive Medicine 2020 Nov (Vol. 38, No. 06, pp. 398-406). Thieme Medical Publishers, Inc.. 5. Dunne F, Newman C, Alvarez-Iglesias A, Ferguson J, Smyth A, Browne M, O’Shea P, Devane D, Gillespie P, Bogdanet D, Kgosidialwa O. Early metformin in gestational diabetes: a randomized clinical trial. Jama. 2023 Oct 24;330(16):1547-56. 6. Elkind-Hirsch KE, Shaler D, Harris R. Postpartum treatment with liraglutide in combination with metformin versus metformin monotherapy to improve metabolic status and reduce body weight in overweight/obese women with recent gestational diabetes: a double-blind, randomized, placebo-controlled study. Journal of Diabetes and its Complications. 2020 Apr 1;34(4):107548. 7. Brzozowska MM, Puvanendran A, Bliuc D, Zuschmann A, Piotrowicz AK, O’Sullivan A. Predictors for pharmacological therapy and perinatal outcomes with metformin treatment in women with gestational diabetes. Frontiers in Endocrinology. 2023 Jan 30;14:1119134. 8. Vajje J, Khan S, Kaur A, Kataria H, Sarpoolaki S, Goudel A, Bhatti AH, Allahwala D. Comparison of the efficacy of metformin and lifestyle modification for the primary prevention of type 2 diabetes: a meta-analysis of randomized controlled trials. Cureus. 2023 Oct 16;15(10). 9. Boggess KA, Valint A, Refuerzo JS, Zork N, Battarbee AN, Eichelberger K, Ramos GA, Olson G, Durnwald C, Landon MB, Aagaard KM. Metformin plus insulin for preexisting diabetes or gestational diabetes in early pregnancy: the MOMPOD randomized clinical trial. Jama. 2023 Dec 12;330(22):2182-90. 10. Yew TW, Chi C, Chan SY, van Dam RM, Whitton C, Lim CS, Foong PS, Fransisca W, Teoh CL, Chen J, Ho-Lim ST. A randomized controlled trial to evaluate the effects of a smartphone application–based lifestyle coaching program on gestational weight gain, glycemic control, and maternal and neonatal outcomes in women with gestational diabetes mellitus: the SMART-GDM study. Diabetes Care. 2021 Feb 1;44(2):456-63. 11. Feig DS. Metformin for diabetes in pregnancy: are we closer to defining its role?. JAMA. 2023 Dec 12;330(22):2167-9. 12. Elkind-Hirsch KE, Seidemann E, Harris R. A randomized trial of dapagliflozin and metformin, alone and combined, in overweight women after gestational diabetes mellitus. American Journal of Obstetrics & Gynecology MFM. 2020 Aug 1;2(3):100139. 13. Mason T, Alesi S, Fernando M, Vanky E, Teede HJ, Mousa A. Metformin in gestational diabetes: physiological actions and clinical applications. Nature Reviews Endocrinology. 2025 Feb;21(2):77-91. 14. Mukherjee SM, Dawson A. Diabetes: how to manage gestational diabetes mellitus. Drugs in context. 2022 Jun 14;11:2021-9. 15. Sagastume D, Siero I, Mertens E, Cottam J, Colizzi C, Peñalvo JL. The effectiveness of lifestyle interventions on type 2 diabetes and gestational diabetes incidence and cardiometabolic outcomes: a systematic review and meta-analysis of evidence from low-and middle-income countries. EClinicalMedicine. 2022 Nov 1;53.