Abnormal glucose regulation occurs in approximately 3-10% of pregnancies. Gestational diabetes mellitus (GDM), defined as glucose intolerance of varying severity with onset or first recognition during pregnancy, accounts for nearly 90% of diabetes mellitus (DM) cases in pregnancy. Rising rates of diabetes, particularly type 2 diabetes, among women of childbearing age in the United States have contributed to an increasing number of pregnant women with preexisting diabetes. Currently, type 2 diabetes accounts for about 8% of diabetes cases in pregnancy, while preexisting diabetes affects nearly 1% of all pregnancies.
Epidemiology
Gestational diabetes mellitus (GDM) is one of the most common complications that arise during pregnancy. The recent data given by the International Diabetes Federation indicate the prevalence of GDM in one out of every six live births across the world. Approximately 7% of all pregnancies in the United States report diabetes wherein GDM occurs approximately 86% of the cases. The percentage of GDM has been estimated as 10.9% in Europe.
Anatomy
Pathophysiology
The increasing concentrations of placental hormones in the presence of the human placental lactogen, estrogen, progesterone, prolactin, and growth hormone during pregnancy are associated with progressive insulin resistance. Growth hormone like properties is especially seen in human placental lactogen which is central to the modification of insulin receptor activity, the diminished uptake of glucose in the periphery, and the maintenance of a constant source of glucose to the fetus. To counter this, maternal insulin secretion increases in normal to maintain euglycemia. The physiologic alterations add to the rationale of screening gestational diabetes mellitus (GDM) during later pregnancy.
The pathophysiology of GDM is very similar to type 2 diabetes, which is an increased insulin resistance and poor secretion of insulin. Impaired β-cell function prevents sufficient compensation, and maternal hyperglycemia occurs due to decreased glucose uptake and increased glucose production by the liver. High levels of glucose in the mother easily pass through the placenta leading to hyperglycemia in the fetus and stimulating the fetal pancreas. The resulting hyperinsulinemia promotes accelerated fetal growth. Additionally, elevated maternal triglyceride levels may exacerbate β-cell dysfunction through lipotoxic effects, further impairing insulin secretion.
Etiology
Hormones produced by the placenta also play a role in increased insulin resistance in pregnancy, specifically human placental lactogen, which impacts resistance while simultaneously stimulating secretion of insulin to ensure glucose homeostasis. In gestational diabetes mellitus, the malfunction or delayed reaction of pancreatic β-cell  leads to insufficient secretion of insulin and hyperglycemia in the mother. Insulin resistance is also increased by maternal obesity increases the level of free fatty acid that inhibits the absorption of glucose and encourages the process of gluconeogenesis in the liver. There is also an indication of genetic association with type 2 diabetes and GDM, with variants in genes that influence insulin release and glucose metabolism (MTNR1B, TCF7L2, HKDC1, GCKR, PPP1R3B and IRS1) associated with both of these conditions.
Genetics
Prognostic Factors
Proper management of glucose during pregnancy reduces cases of complications like macrosomia, newborn hypoglycemia and preeclampsia and the risk of preeclampsia is reduced by 18 to 12 cases when drugs are administered. Lifestyle modifications or pharmacologic therapy can help decrease the 10-year risk of developing type-2 diabetes by a factor of 35 to 40. Even small weight loss is correlated with a reduction of diabetes by 25%.
Clinical History
Age group
Gestational diabetes may develop at any reproductive age, yet the chances of developing this condition are high with maternal age. Prevalence is greater among women above the age of 25 years, and the prevalence rises after 35 years of age. The advanced maternal age can be a major risk factor of GDM, which is combined with obesity, familial diabetes history, and the past pregnancy negative experience.
Physical Examination
Gestational diabetes mellitus (GDM) is best identified by screening in the course of pregnancy. Clinical history guides early assessment and, therefore, recording of previous medical history, previous obstetric outcome, and family history of type 2 diabetes can be considered an important aspect of assessment. The manifestation of GDM may differ, but some symptoms include excessive weight gain, obesity, and increased body mass index (BMI), which are usually suggestive.
Age group
Associated comorbidity
Hypertension and preeclampsia
Obesity and metabolic syndrome
Dyslipidemia and elevated triglycerides
Polycystic ovary syndrome (PCOS)
Increased long-term risk of type 2 diabetes mellitus and cardiovascular disease
Associated activity
Acuity of presentation
The onset of GDM is usually slow and is mostly asymptomatic, discovered by routine screening in the second or third trimester. In comparison to type 1 diabetes, it rarely presents with acute symptoms as polyuria, polydipsia, or weight loss. Nevertheless, in case of a significant increase in blood glucose levels, some women may experience fatigue, excessive thirst, or recurrent infections. Acute presentations are uncommon, and diagnosis is primarily based on screening rather than symptoms.
Differential Diagnoses
Many women do not get screened for diabetes before pregnancy, and it may be unclear whether they have gestational diabetes mellitus (GDM) rather than type 2 diabetes or maturity-onset diabetes of the young (MODY).
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Nonpharmacologic Therapies
Lifestyle interventions
Treatment of gestational diabetes mellitus (GDM) starts with lifestyle modifications, such as exercise, diet and glucose level measurement, patients are advised to engage in 150 minutes of moderate-intensity aerobic exercise per week preferably 30 minutes daily on most days. Postprandial exercise is commonly advised, as this exercise can be used to improve the control of glucose up to 3 hours following meals.
Dietary modifications
Both ADA and ACOG recommend individualized nutrition counseling, preferably with a dietitian, to balance caloric needs with appropriate weight gain. Key strategies include:
Three small-to-moderate meals plus 2-3 snacks daily.
Emphasis on whole-grain carbohydrates, lean protein, and unsaturated fats.
Reduced carbohydrate intake at breakfast due to morning carbohydrate intolerance.
Bedtime snack to prevent nocturnal ketosis and protect fetal neurodevelopment.
Although the optimal macronutrient ratio is unclear, combining carbohydrates with lean protein may reduce postprandial hyperglycemia.
Pharmacologic Therapies
If lifestyle measures fail to achieve glycemic control, pharmacologic therapy is required. Insulin is the preferred treatment, though oral agents are sometimes used off-label.
Insulin therapy
Insulin does not cross the placenta and is recommended as first-line therapy by the ADA. Regimens typically combine basal insulin (to control fasting glucose) with short-acting insulin (to address postprandial hyperglycemia). Initial doses are calculated based on maternal weight and gestational age, then adjusted according to glucose logs.
Focus on balanced meals with controlled carbohydrate intake, emphasizing complex carbohydrates, high fiber foods, lean proteins, and healthy fats.
Small, frequent meals and snacks help prevent glucose spikes.
Avoidance of refined sugars and processed foods is recommended.
Weight Management:
For women who are overweight or obese, careful monitoring of gestational weight gain is essential.
Target weight gain is based on pre-pregnancy BMI, in line with Institute of Medicine (IOM) guidelines.
Physical Activity:
Moderate-intensity exercise (e.g., walking, swimming, prenatal yoga) for 30 minutes most days of the week improves insulin sensitivity and glucose utilization.
Activity should be tailored to maternal health status and pregnancy safety.
Lifestyle Counseling and Monitoring:
Education on healthy eating habits, portion control, and physical activity is vital.
Self-monitoring of blood glucose (SMBG) guides dietary and activity adjustments.
Behavioral Support:
Stress reduction, adequate sleep, and structured daily routines contribute to better glycemic control.
Effectiveness of oral hypoglycemic agents in treating gestational diabetes
Oral Hypoglycemic Agents
Metformin
Metformin is initiated at 500 mg once daily for the first week, and while it is tolerable to increase to 1,000 mg twice daily subsequently, the maximum dose is 2,500-3,000 mg. Metformin readily crosses the placental barrier and is associated with maternal gastrointestinal discomfort and diarrhea. It has also been noted that metformin may increase risks of preterm delivery. Metformin and insulin have comparable outcomes with respect to macrosomia, neonatal hypoglycemia, and cesarean delivery.
Glyburide
Glyburide is usually initiated at 2.5mg per day with the possibility of increasing to as much as 20mg, but it is shown to be less effective than insulin. As a restriction to prior understanding, glyburide is known to cross the placenta and is associated with increased rates of several poor outcomes, including admissions to the neonatal intensive care unit, respiratory distress, hypoglycemia, birth trauma, and the potential for fetal stimulation of insulin. This has led to ACOG’s (American College of Obstetrics and Gynecology) recommendation that glyburide is not used as a first-line option.
Role of insulin in treating gestational diabetes
Insulin is considered the first-line therapy for gestational diabetes and is preferred by both the ADA and ACOG because it does not cross the placenta. Treatment typically involves a combination of basal insulin to manage fasting hyperglycemia and short-acting insulin to control postprandial glucose levels. The initial dose is calculated according to maternal weight and gestational age and is later adjusted based on glucose monitoring. Insulin therapy is flexible, effective, and safe for use throughout pregnancy.
Abnormal glucose regulation occurs in approximately 3-10% of pregnancies. Gestational diabetes mellitus (GDM), defined as glucose intolerance of varying severity with onset or first recognition during pregnancy, accounts for nearly 90% of diabetes mellitus (DM) cases in pregnancy. Rising rates of diabetes, particularly type 2 diabetes, among women of childbearing age in the United States have contributed to an increasing number of pregnant women with preexisting diabetes. Currently, type 2 diabetes accounts for about 8% of diabetes cases in pregnancy, while preexisting diabetes affects nearly 1% of all pregnancies.
Gestational diabetes mellitus (GDM) is one of the most common complications that arise during pregnancy. The recent data given by the International Diabetes Federation indicate the prevalence of GDM in one out of every six live births across the world. Approximately 7% of all pregnancies in the United States report diabetes wherein GDM occurs approximately 86% of the cases. The percentage of GDM has been estimated as 10.9% in Europe.
The increasing concentrations of placental hormones in the presence of the human placental lactogen, estrogen, progesterone, prolactin, and growth hormone during pregnancy are associated with progressive insulin resistance. Growth hormone like properties is especially seen in human placental lactogen which is central to the modification of insulin receptor activity, the diminished uptake of glucose in the periphery, and the maintenance of a constant source of glucose to the fetus. To counter this, maternal insulin secretion increases in normal to maintain euglycemia. The physiologic alterations add to the rationale of screening gestational diabetes mellitus (GDM) during later pregnancy.
The pathophysiology of GDM is very similar to type 2 diabetes, which is an increased insulin resistance and poor secretion of insulin. Impaired β-cell function prevents sufficient compensation, and maternal hyperglycemia occurs due to decreased glucose uptake and increased glucose production by the liver. High levels of glucose in the mother easily pass through the placenta leading to hyperglycemia in the fetus and stimulating the fetal pancreas. The resulting hyperinsulinemia promotes accelerated fetal growth. Additionally, elevated maternal triglyceride levels may exacerbate β-cell dysfunction through lipotoxic effects, further impairing insulin secretion.
Hormones produced by the placenta also play a role in increased insulin resistance in pregnancy, specifically human placental lactogen, which impacts resistance while simultaneously stimulating secretion of insulin to ensure glucose homeostasis. In gestational diabetes mellitus, the malfunction or delayed reaction of pancreatic β-cell  leads to insufficient secretion of insulin and hyperglycemia in the mother. Insulin resistance is also increased by maternal obesity increases the level of free fatty acid that inhibits the absorption of glucose and encourages the process of gluconeogenesis in the liver. There is also an indication of genetic association with type 2 diabetes and GDM, with variants in genes that influence insulin release and glucose metabolism (MTNR1B, TCF7L2, HKDC1, GCKR, PPP1R3B and IRS1) associated with both of these conditions.
Proper management of glucose during pregnancy reduces cases of complications like macrosomia, newborn hypoglycemia and preeclampsia and the risk of preeclampsia is reduced by 18 to 12 cases when drugs are administered. Lifestyle modifications or pharmacologic therapy can help decrease the 10-year risk of developing type-2 diabetes by a factor of 35 to 40. Even small weight loss is correlated with a reduction of diabetes by 25%.
Age group
Gestational diabetes may develop at any reproductive age, yet the chances of developing this condition are high with maternal age. Prevalence is greater among women above the age of 25 years, and the prevalence rises after 35 years of age. The advanced maternal age can be a major risk factor of GDM, which is combined with obesity, familial diabetes history, and the past pregnancy negative experience.
Gestational diabetes mellitus (GDM) is best identified by screening in the course of pregnancy. Clinical history guides early assessment and, therefore, recording of previous medical history, previous obstetric outcome, and family history of type 2 diabetes can be considered an important aspect of assessment. The manifestation of GDM may differ, but some symptoms include excessive weight gain, obesity, and increased body mass index (BMI), which are usually suggestive.
Hypertension and preeclampsia
Obesity and metabolic syndrome
Dyslipidemia and elevated triglycerides
Polycystic ovary syndrome (PCOS)
Increased long-term risk of type 2 diabetes mellitus and cardiovascular disease
The onset of GDM is usually slow and is mostly asymptomatic, discovered by routine screening in the second or third trimester. In comparison to type 1 diabetes, it rarely presents with acute symptoms as polyuria, polydipsia, or weight loss. Nevertheless, in case of a significant increase in blood glucose levels, some women may experience fatigue, excessive thirst, or recurrent infections. Acute presentations are uncommon, and diagnosis is primarily based on screening rather than symptoms.
Many women do not get screened for diabetes before pregnancy, and it may be unclear whether they have gestational diabetes mellitus (GDM) rather than type 2 diabetes or maturity-onset diabetes of the young (MODY).
Nonpharmacologic Therapies
Lifestyle interventions
Treatment of gestational diabetes mellitus (GDM) starts with lifestyle modifications, such as exercise, diet and glucose level measurement, patients are advised to engage in 150 minutes of moderate-intensity aerobic exercise per week preferably 30 minutes daily on most days. Postprandial exercise is commonly advised, as this exercise can be used to improve the control of glucose up to 3 hours following meals.
Dietary modifications
Both ADA and ACOG recommend individualized nutrition counseling, preferably with a dietitian, to balance caloric needs with appropriate weight gain. Key strategies include:
Three small-to-moderate meals plus 2-3 snacks daily.
Emphasis on whole-grain carbohydrates, lean protein, and unsaturated fats.
Reduced carbohydrate intake at breakfast due to morning carbohydrate intolerance.
Bedtime snack to prevent nocturnal ketosis and protect fetal neurodevelopment.
Although the optimal macronutrient ratio is unclear, combining carbohydrates with lean protein may reduce postprandial hyperglycemia.
Pharmacologic Therapies
If lifestyle measures fail to achieve glycemic control, pharmacologic therapy is required. Insulin is the preferred treatment, though oral agents are sometimes used off-label.
Insulin therapy
Insulin does not cross the placenta and is recommended as first-line therapy by the ADA. Regimens typically combine basal insulin (to control fasting glucose) with short-acting insulin (to address postprandial hyperglycemia). Initial doses are calculated based on maternal weight and gestational age, then adjusted according to glucose logs.
Endocrinology, Metabolism
Medical Nutrition Therapy (MNT):
Diet is the cornerstone of GDM management.
Focus on balanced meals with controlled carbohydrate intake, emphasizing complex carbohydrates, high fiber foods, lean proteins, and healthy fats.
Small, frequent meals and snacks help prevent glucose spikes.
Avoidance of refined sugars and processed foods is recommended.
Weight Management:
For women who are overweight or obese, careful monitoring of gestational weight gain is essential.
Target weight gain is based on pre-pregnancy BMI, in line with Institute of Medicine (IOM) guidelines.
Physical Activity:
Moderate-intensity exercise (e.g., walking, swimming, prenatal yoga) for 30 minutes most days of the week improves insulin sensitivity and glucose utilization.
Activity should be tailored to maternal health status and pregnancy safety.
Lifestyle Counseling and Monitoring:
Education on healthy eating habits, portion control, and physical activity is vital.
Self-monitoring of blood glucose (SMBG) guides dietary and activity adjustments.
Behavioral Support:
Stress reduction, adequate sleep, and structured daily routines contribute to better glycemic control.
Endocrinology, Metabolism
Oral Hypoglycemic Agents
Metformin
Metformin is initiated at 500 mg once daily for the first week, and while it is tolerable to increase to 1,000 mg twice daily subsequently, the maximum dose is 2,500-3,000 mg. Metformin readily crosses the placental barrier and is associated with maternal gastrointestinal discomfort and diarrhea. It has also been noted that metformin may increase risks of preterm delivery. Metformin and insulin have comparable outcomes with respect to macrosomia, neonatal hypoglycemia, and cesarean delivery.
Glyburide
Glyburide is usually initiated at 2.5mg per day with the possibility of increasing to as much as 20mg, but it is shown to be less effective than insulin. As a restriction to prior understanding, glyburide is known to cross the placenta and is associated with increased rates of several poor outcomes, including admissions to the neonatal intensive care unit, respiratory distress, hypoglycemia, birth trauma, and the potential for fetal stimulation of insulin. This has led to ACOG’s (American College of Obstetrics and Gynecology) recommendation that glyburide is not used as a first-line option.
Endocrinology, Metabolism
Insulin is considered the first-line therapy for gestational diabetes and is preferred by both the ADA and ACOG because it does not cross the placenta. Treatment typically involves a combination of basal insulin to manage fasting hyperglycemia and short-acting insulin to control postprandial glucose levels. The initial dose is calculated according to maternal weight and gestational age and is later adjusted based on glucose monitoring. Insulin therapy is flexible, effective, and safe for use throughout pregnancy.
Endocrinology, Metabolism
Screening and Diagnosis
Risk-based or universal screening (24–28 weeks).
Early testing in high-risk women.
Initial Management (Lifestyle)
Medical nutrition therapy, weight control, and exercise.
Self-monitoring of blood glucose (SMBG).
Pharmacologic Therapy
Insulin as first-line if targets not met.
Metformin or glyburide as alternatives in selected cases.
Monitoring During Pregnancy
Regular glucose checks and fetal growth surveillance.
Adjust therapy with advancing gestation.
Intrapartum Management
Maintain maternal euglycemia during labor.
Insulin/glucose infusions as needed.
Postpartum Care
Reassess glucose tolerance after delivery.
Long-term follow-up to reduce risk of type 2 diabetes.
Abnormal glucose regulation occurs in approximately 3-10% of pregnancies. Gestational diabetes mellitus (GDM), defined as glucose intolerance of varying severity with onset or first recognition during pregnancy, accounts for nearly 90% of diabetes mellitus (DM) cases in pregnancy. Rising rates of diabetes, particularly type 2 diabetes, among women of childbearing age in the United States have contributed to an increasing number of pregnant women with preexisting diabetes. Currently, type 2 diabetes accounts for about 8% of diabetes cases in pregnancy, while preexisting diabetes affects nearly 1% of all pregnancies.
Gestational diabetes mellitus (GDM) is one of the most common complications that arise during pregnancy. The recent data given by the International Diabetes Federation indicate the prevalence of GDM in one out of every six live births across the world. Approximately 7% of all pregnancies in the United States report diabetes wherein GDM occurs approximately 86% of the cases. The percentage of GDM has been estimated as 10.9% in Europe.
The increasing concentrations of placental hormones in the presence of the human placental lactogen, estrogen, progesterone, prolactin, and growth hormone during pregnancy are associated with progressive insulin resistance. Growth hormone like properties is especially seen in human placental lactogen which is central to the modification of insulin receptor activity, the diminished uptake of glucose in the periphery, and the maintenance of a constant source of glucose to the fetus. To counter this, maternal insulin secretion increases in normal to maintain euglycemia. The physiologic alterations add to the rationale of screening gestational diabetes mellitus (GDM) during later pregnancy.
The pathophysiology of GDM is very similar to type 2 diabetes, which is an increased insulin resistance and poor secretion of insulin. Impaired β-cell function prevents sufficient compensation, and maternal hyperglycemia occurs due to decreased glucose uptake and increased glucose production by the liver. High levels of glucose in the mother easily pass through the placenta leading to hyperglycemia in the fetus and stimulating the fetal pancreas. The resulting hyperinsulinemia promotes accelerated fetal growth. Additionally, elevated maternal triglyceride levels may exacerbate β-cell dysfunction through lipotoxic effects, further impairing insulin secretion.
Hormones produced by the placenta also play a role in increased insulin resistance in pregnancy, specifically human placental lactogen, which impacts resistance while simultaneously stimulating secretion of insulin to ensure glucose homeostasis. In gestational diabetes mellitus, the malfunction or delayed reaction of pancreatic β-cell  leads to insufficient secretion of insulin and hyperglycemia in the mother. Insulin resistance is also increased by maternal obesity increases the level of free fatty acid that inhibits the absorption of glucose and encourages the process of gluconeogenesis in the liver. There is also an indication of genetic association with type 2 diabetes and GDM, with variants in genes that influence insulin release and glucose metabolism (MTNR1B, TCF7L2, HKDC1, GCKR, PPP1R3B and IRS1) associated with both of these conditions.
Proper management of glucose during pregnancy reduces cases of complications like macrosomia, newborn hypoglycemia and preeclampsia and the risk of preeclampsia is reduced by 18 to 12 cases when drugs are administered. Lifestyle modifications or pharmacologic therapy can help decrease the 10-year risk of developing type-2 diabetes by a factor of 35 to 40. Even small weight loss is correlated with a reduction of diabetes by 25%.
Age group
Gestational diabetes may develop at any reproductive age, yet the chances of developing this condition are high with maternal age. Prevalence is greater among women above the age of 25 years, and the prevalence rises after 35 years of age. The advanced maternal age can be a major risk factor of GDM, which is combined with obesity, familial diabetes history, and the past pregnancy negative experience.
Gestational diabetes mellitus (GDM) is best identified by screening in the course of pregnancy. Clinical history guides early assessment and, therefore, recording of previous medical history, previous obstetric outcome, and family history of type 2 diabetes can be considered an important aspect of assessment. The manifestation of GDM may differ, but some symptoms include excessive weight gain, obesity, and increased body mass index (BMI), which are usually suggestive.
Hypertension and preeclampsia
Obesity and metabolic syndrome
Dyslipidemia and elevated triglycerides
Polycystic ovary syndrome (PCOS)
Increased long-term risk of type 2 diabetes mellitus and cardiovascular disease
The onset of GDM is usually slow and is mostly asymptomatic, discovered by routine screening in the second or third trimester. In comparison to type 1 diabetes, it rarely presents with acute symptoms as polyuria, polydipsia, or weight loss. Nevertheless, in case of a significant increase in blood glucose levels, some women may experience fatigue, excessive thirst, or recurrent infections. Acute presentations are uncommon, and diagnosis is primarily based on screening rather than symptoms.
Many women do not get screened for diabetes before pregnancy, and it may be unclear whether they have gestational diabetes mellitus (GDM) rather than type 2 diabetes or maturity-onset diabetes of the young (MODY).
Nonpharmacologic Therapies
Lifestyle interventions
Treatment of gestational diabetes mellitus (GDM) starts with lifestyle modifications, such as exercise, diet and glucose level measurement, patients are advised to engage in 150 minutes of moderate-intensity aerobic exercise per week preferably 30 minutes daily on most days. Postprandial exercise is commonly advised, as this exercise can be used to improve the control of glucose up to 3 hours following meals.
Dietary modifications
Both ADA and ACOG recommend individualized nutrition counseling, preferably with a dietitian, to balance caloric needs with appropriate weight gain. Key strategies include:
Three small-to-moderate meals plus 2-3 snacks daily.
Emphasis on whole-grain carbohydrates, lean protein, and unsaturated fats.
Reduced carbohydrate intake at breakfast due to morning carbohydrate intolerance.
Bedtime snack to prevent nocturnal ketosis and protect fetal neurodevelopment.
Although the optimal macronutrient ratio is unclear, combining carbohydrates with lean protein may reduce postprandial hyperglycemia.
Pharmacologic Therapies
If lifestyle measures fail to achieve glycemic control, pharmacologic therapy is required. Insulin is the preferred treatment, though oral agents are sometimes used off-label.
Insulin therapy
Insulin does not cross the placenta and is recommended as first-line therapy by the ADA. Regimens typically combine basal insulin (to control fasting glucose) with short-acting insulin (to address postprandial hyperglycemia). Initial doses are calculated based on maternal weight and gestational age, then adjusted according to glucose logs.
Endocrinology, Metabolism
Medical Nutrition Therapy (MNT):
Diet is the cornerstone of GDM management.
Focus on balanced meals with controlled carbohydrate intake, emphasizing complex carbohydrates, high fiber foods, lean proteins, and healthy fats.
Small, frequent meals and snacks help prevent glucose spikes.
Avoidance of refined sugars and processed foods is recommended.
Weight Management:
For women who are overweight or obese, careful monitoring of gestational weight gain is essential.
Target weight gain is based on pre-pregnancy BMI, in line with Institute of Medicine (IOM) guidelines.
Physical Activity:
Moderate-intensity exercise (e.g., walking, swimming, prenatal yoga) for 30 minutes most days of the week improves insulin sensitivity and glucose utilization.
Activity should be tailored to maternal health status and pregnancy safety.
Lifestyle Counseling and Monitoring:
Education on healthy eating habits, portion control, and physical activity is vital.
Self-monitoring of blood glucose (SMBG) guides dietary and activity adjustments.
Behavioral Support:
Stress reduction, adequate sleep, and structured daily routines contribute to better glycemic control.
Endocrinology, Metabolism
Oral Hypoglycemic Agents
Metformin
Metformin is initiated at 500 mg once daily for the first week, and while it is tolerable to increase to 1,000 mg twice daily subsequently, the maximum dose is 2,500-3,000 mg. Metformin readily crosses the placental barrier and is associated with maternal gastrointestinal discomfort and diarrhea. It has also been noted that metformin may increase risks of preterm delivery. Metformin and insulin have comparable outcomes with respect to macrosomia, neonatal hypoglycemia, and cesarean delivery.
Glyburide
Glyburide is usually initiated at 2.5mg per day with the possibility of increasing to as much as 20mg, but it is shown to be less effective than insulin. As a restriction to prior understanding, glyburide is known to cross the placenta and is associated with increased rates of several poor outcomes, including admissions to the neonatal intensive care unit, respiratory distress, hypoglycemia, birth trauma, and the potential for fetal stimulation of insulin. This has led to ACOG’s (American College of Obstetrics and Gynecology) recommendation that glyburide is not used as a first-line option.
Endocrinology, Metabolism
Insulin is considered the first-line therapy for gestational diabetes and is preferred by both the ADA and ACOG because it does not cross the placenta. Treatment typically involves a combination of basal insulin to manage fasting hyperglycemia and short-acting insulin to control postprandial glucose levels. The initial dose is calculated according to maternal weight and gestational age and is later adjusted based on glucose monitoring. Insulin therapy is flexible, effective, and safe for use throughout pregnancy.
Endocrinology, Metabolism
Screening and Diagnosis
Risk-based or universal screening (24–28 weeks).
Early testing in high-risk women.
Initial Management (Lifestyle)
Medical nutrition therapy, weight control, and exercise.
Self-monitoring of blood glucose (SMBG).
Pharmacologic Therapy
Insulin as first-line if targets not met.
Metformin or glyburide as alternatives in selected cases.
Monitoring During Pregnancy
Regular glucose checks and fetal growth surveillance.
Adjust therapy with advancing gestation.
Intrapartum Management
Maintain maternal euglycemia during labor.
Insulin/glucose infusions as needed.
Postpartum Care
Reassess glucose tolerance after delivery.
Long-term follow-up to reduce risk of type 2 diabetes.
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