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Cited by 928Gestational Diabetes Research and ManagementBirth, Development, and HealthDiabetes, Cardiovascular Risks, and Lipoproteins

A Clinical Update on Gestational Diabetes Mellitus

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Sweeting, Arianne, Wong, Jencia, Murphy, Helen R, Ross, Glynis P·2022·Endocrine Reviews
DOI 10.1210/endrev/bnac003PMC PMC9512153
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Abstract

Gestational diabetes mellitus (GDM) traditionally refers to abnormal glucose tolerance with onset or first recognition during pregnancy. GDM has long been associated with obstetric and neonatal complications primarily relating to higher infant birthweight and is increasingly recognized as a risk factor for future maternal and offspring cardiometabolic disease. The prevalence of GDM continues to rise internationally due to epidemiological factors including the increase in background rates of obesity in women of reproductive age and rising maternal age and the implementation of the revised International Association of the Diabetes and Pregnancy Study Groups’ criteria and diagnostic procedures for GDM. The current lack of international consensus for the diagnosis of GDM reflects its complex historical evolution and pragmatic antenatal resource considerations given GDM is now 1 of the most common complications of pregnancy. Regardless, the contemporary clinical approach to GDM should be informed not only by its short-term complications but also by its longer term prognosis. Recent data demonstrate the effect of early in utero exposure to maternal hyperglycemia, with evidence for fetal overgrowth present prior to the traditional diagnosis of GDM from 24 weeks’ gestation, as well as the durable adverse impact of maternal hyperglycemia on child and adolescent metabolism. The major contribution of GDM to the global epidemic of intergenerational cardiometabolic disease highlights the importance of identifying GDM as an early risk factor for type 2 diabetes and cardiovascular disease, broadening the prevailing clinical approach to address longer term maternal and offspring complications following a diagnosis of GDM.

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  • Early diagnosis of GDM is crucial because it predisposes offspring to early development of type 2 diabetes and cardiovascular diseases and allows timely improvement of clinical management.

    “In light of this evidence, early diagnosis of gestational diabetes mellitus (GDM) is crucial, as it predisposes offspring to the early development of type 2 diabetes and cardiovascular diseases and allows for the timely improvement and optimization of clinical management and therapeutic interventions [31,32,33,34].”

    From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [31]

    The Abstract and “Long-term Risk in the Offspring” section link GDM to future type 2 diabetes and cardiovascular risk in offspring, including early-onset cardiovascular disease. But the “Early GDM” section says high-quality evidence is lacking that diagnosing and treating GDM early improves pregnancy outcomes. The source therefore supports the offspring-risk rationale and the value of detecting GDM, but not the unqualified claim that early diagnosis enables improved management and outcomes. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • In late gestation, insulin sensitivity is reduced by 40-80% in gravidae with normal or elevated body mass index.

    “Evidence from late-gestation studies demonstrates that insulin sensitivity is reduced by 40–80% in gravidae with normal or elevated body mass index.”

    From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [31]

    The Pathophysiology of GDM section reports a 40–80% decrease by late pregnancy in women with normal or increased BMI, but calls the measured quantity maternal glucose sensitivity, not insulin sensitivity. The same passage describes increasing insulin resistance, supporting the claim’s general direction but not its precise attribution of the percentage. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • Maternal glucose elevation has inverse associations with offspring insulin sensitivity and HOMA indices at 14 years, persisting after adjustment for maternal BMI, offspring BMI, and familial diabetes predisposition.

    “Conversely, maternal glucose elevation demonstrated inverse associations with offspring insulin sensitivity and homeostatic model assessment (HOMA) indices at 14 years, with these relationships persisting after statistical adjustment for maternal body mass index, offspring BMI, and familial diabetes predisposition.”

    From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [31]

    The “Long-term Risk in the Offspring” section reports inverse associations of maternal glucose with offspring insulin sensitivity and disposition index by age 14, independent of maternal and childhood BMI and family history of diabetes. The claim substitutes HOMA indices for disposition index; the cited passage does not report an inverse association with HOMA indices. (LLM, conf=0.90)

    Experimental — accuracy not yet measured

  • In women diagnosed with gestational diabetes mellitus, blood glucose levels return to normal following delivery.

    “In women diagnosed with GDM, blood glucose levels return to normal following delivery [54]”

    From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [54]

    The “Longer Term Management of Women Following GDM” section indicates that many women have normal postpartum glucose levels, but reports that up to one third have levels consistent with diabetes or prediabetes at 6–12 weeks. The claim overstates this as a return to normal for women with GDM generally. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • Normal pregnancy is associated with a progressive increase in insulin resistance predominantly due to increased circulating placental hormones including growth hormone, corticotrophin-releasing hormone, human placental lactogen, prolactin, estrogen, and progesterone.

    “There is a progressive increase in insulin resistance, predominantly due to increased circulating placental hormones, including growth hormone, corticotrophin-releasing hormone, human placental lactogen, prolactin, estrogen, and progesterone.”

    From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [31]

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Authors
Sweeting, A., Wong, J., Murphy, H. R., & Ross, G. P.
Affiliations
  • The University of Sydney (AU)
  • University of East Anglia (GB)
Corresponding author
Sweeting, Arianne
ORCID
Venue
Endocrine Reviews
Publisher
The Endocrine Society
Published
2022-01-18
Volume
43
Issue
5
Pages
763-793
ISSN
  • 0163-769X (ISSN-L)
  • 1945-7189
DOI
10.1210/endrev/bnac003
PMC
PMC9512153
OpenAlex
W4205324281
Cited by
928
References
55
Citations by year
2026: 219 · 2025: 308 · 2024: 255 · 2023: 136 · 2022: 10
FWCI
178.60
Type
journal article
Language
en
Open access
Licence
Locations
  • Endocrine Reviews (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • Research Portal (King's College London) (publishedVersion, other-oa)
Funders
NHMRC (GNT1148952)
Topics
  • Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords
gestational diabetes mellitus, maternal hyperglycemia, fetal overgrowth, neonatal complications, cardiometabolic disease, type 2 diabetes risk, cardiovascular risk, IADPSG criteria, GDM prevalence, maternal obesity, long-term prognosis
MeSH terms
Adolescent, Cardiovascular Diseases, Child, Diabetes Mellitus, Type 2, Female, Fetal Macrosomia, Glucose, Humans, Hyperglycemia, Infant, Newborn, Pregnancy, Diabetes, Gestational

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