Trying to understand gestational diabetes
Open accessAbstract
Women with normal glucose tolerance pre‐gravid and developing gestational diabetes in late gestation have subclinical metabolic dysfunction prior to conception compared with women with normal glucose tolerance. Because of the 60% decrease in insulin sensitivity with normal pregnancy, these women develop clinical hyperglycaemia/gestational diabetes in late gestation. The metabolic dysfunction includes impaired insulin response, decreased hepatic suppression of glucose production during insulin infusion and decreased insulin‐stimulated glucose uptake in skeletal muscle, i.e. peripheral insulin resistance. The insulin resistance in normal glucose tolerance pregnancy is related to a decrease in the post‐receptor insulin signalling cascade, specifically decreased insulin receptor substrate 1 tyrosine phosphorylation. In women with normal glucose tolerance this is reversed post‐partum. In contrast, in gestational diabetes, in addition to the decrease in insulin receptor substrate 1 tyrosine phosphorylation, there is an additional decrease in tyrosine phosphorylation of the intracellular portion of the insulin receptor that is not related to the insulin receptor protein content. Post‐partum women with gestational diabetes, who had retention of gestational weight gain, had no significant improvement in insulin sensitivity and increased inflammation expressed as increased plasma and skeletal muscle tumour necrosis factor alpha. The increased inflammation or meta‐inflammation is a hallmark of obesity and during pregnancy develops in both white adipose tissue and placenta. Last gene array studies of placenta were associated with alterations in gene expression relating primarily to lipid in contrast to glucose metabolic pathways in gestational diabetes compared with Type 1 diabetes. Future studies are directed at decreasing inflammation prior to and during pregnancy using various lifestyle and nutritional interventions.
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Altered expression and/or phosphorylation of IRS-1, PI3K, and GLUT4 has been described in GDM.
“In addition, altered expression and/or phosphorylation of downstream regulators of insulin signaling, including insulin receptor substrate (IRS)-1, phosphatidylinositol 3-kinase (PI3K), and GLUT4, has been described in GDM [84].”
From The Pathophysiology of Gestational Diabetes Mellitus (2018) · cites this paper as [84]
The section “Endogenous glucose production and suppression during pregnancy” (page unavailable) reports reduced IRS-1 protein content and tyrosine phosphorylation in GDM, as well as increased expression of a PI3K regulatory subunit. It does not describe altered GLUT4 expression or phosphorylation; the reported reduction in glucose transport does not establish that part of the claim. (LLM, conf=0.87)
Experimental — accuracy not yet measuredGDM is associated with upregulated hepatic glucose production (gluconeogenesis).
“GDM is associated with upregulated hepatic glucose production (gluconeogenesis).”
From The Pathophysiology of Gestational Diabetes Mellitus (2018) · cites this paper as [84]
The “Endogenous glucose production and suppression during pregnancy” section (page not available) reports less suppression of hepatic glucose production during insulin infusion in women with GDM. But basal production rose similarly in women with and without GDM, with no significant difference between groups. The passage measures endogenous glucose production; it does not specifically establish increased gluconeogenesis. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe rate of insulin-stimulated glucose uptake is reduced by 54% in GDM when compared with normal pregnancy.
“The rate of insulin-stimulated glucose uptake is reduced by 54% in GDM when compared with normal pregnancy [84].”
From The Pathophysiology of Gestational Diabetes Mellitus (2018) · cites this paper as [84]
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Cites
Glucose clamp technique: a method for quantifying insulin secretion and resistance.
DeFronzo, R. A., Tobin, J. D., & Andres, R. (1979) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1979.237.3.e214 · Cited by 7,425 · see citing works
Hotamisligil, G. S., Peraldi, P., Budavari, A., Ellis, R., White, M. F., & Spiegelman, B. M. (1996) · Science · doi:10.1126/science.271.5249.665 · Cited by 2,630 · see citing works
Techniques for Measuring Body Composition
National Research Council (1961) · National Academies Press eBooks · doi:10.17226/21603 · Cited by 1,616 · see citing works
Banting lecture 1980: of pregnancy and progeny.
Freinkel, N. (1980) · Diabetes · doi:10.2337/diab.29.12.1023 · Cited by 1,366 · see citing works
The Hyperglycemia and Adverse Pregnancy Outcome Study
Catalano, P. M., McIntyre, H. D., Cruickshank, J. K., McCance, D. R., Dyer, A. R., Metzger, B. E., Lowe, L. P., Trimble, E. R., Coustan, D. R., Hadden, D. R., et al. (2012) · Diabetes Care · doi:10.2337/dc11-1790 · Cited by 954 · see citing works
Self-citationKeys, A. B., & Brožek, J. (1953) · Physiological Reviews · doi:10.1152/physrev.1953.33.3.245 · Cited by 858 · see citing works
TNF-α Is a Predictor of Insulin Resistance in Human Pregnancy
Kirwan, J. P., Hauguel-De Mouzon, S., Lepercq, J., Challier, J.-C., Huston-Presley, L., Friedman, J. E., Kalhan, S. C., & Catalano, P. M. (2002) · Diabetes · doi:10.2337/diabetes.51.7.2207 · Cited by 738 · see citing works
Self-citationObesity in Pregnancy Stimulates Macrophage Accumulation and Inflammation in the Placenta
Challier, J. C., Basu, S., Bintein, T., Minium, J., Hotmire, K., Catalano, P. M., & Hauguel-de Mouzon, S. (2008) · Placenta · doi:10.1016/j.placenta.2007.12.010 · Cited by 712 · see citing works
Self-citationCatalano, P. M., Huston, L., Amini, S. B., & Kalhan, S. C. (1999) · American Journal of Obstetrics and Gynecology · doi:10.1016/s0002-9378(99)70662-9 · Cited by 680 · see citing works
Self-citationCarbohydrate metabolism during pregnancy in control subjects and women with gestational diabetes
Catalano, P. M., Tyzbir, E. D., Wolfe, R. R., Calles, J., Roman, N. M., Amini, S. B., & Sims, E. A. (1993) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1993.264.1.e60 · Cited by 484 · see citing works
Self-citationGestational Diabetes Induces Placental Genes for Chronic Stress and Inflammatory Pathways
Radaelli, T., Varastehpour, A., Catalano, P., & Hauguel-de Mouzon, S. (2003) · Diabetes · doi:10.2337/diabetes.52.12.2951 · Cited by 390 · see citing works
Self-citationIs it time to revisit the Pedersen hypothesis in the face of the obesity epidemic?
Catalano, P. M., & Mouzon, S. H. (2011) · American Journal of Obstetrics and Gynecology · doi:10.1016/j.ajog.2010.11.039 · Cited by 331 · see citing works
Self-citationThe Placenta Cytokine Network and Inflammatory Signals
Mouzon, S. H., & Guerre-Millo, M. (2005) · Placenta · doi:10.1016/j.placenta.2005.08.009 · Cited by 294 · see citing works
Friedman, J. E., Ishizuka, T., Shao, J., Huston, L., Highman, T., & Catalano, P. (1999) · Diabetes · doi:10.2337/diabetes.48.9.1807 · Cited by 255 · see citing works
Self-citationCatalano, P. M., Roman-Drago, N. M., Amini, S. B., & Sims, E. A. H. (1998) · American Journal of Obstetrics and Gynecology · doi:10.1016/s0002-9378(98)70267-4 · Cited by 159 · see citing works
Self-citationRadaelli, T., Lepercq, J., Varastehpour, A., Basu, S., Catalano, P. M., & Hauguel-De Mouzon, S. (2009) · American Journal of Obstetrics and Gynecology · doi:10.1016/j.ajog.2009.04.019 · Cited by 156 · see citing works
Self-citationInsulin Receptors in Human and Animal Placental Tissue
Posner, B. I. (1974) · Diabetes · doi:10.2337/diab.23.3.209 · Cited by 155 · see citing works
Okereke, N. C., Huston-Presley, L., Amini, S. B., Kalhan, S. C., & Catalano, P. M. (2004) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00589.2003 · Cited by 98 · see citing works
Self-citationFriedman, J. E., Kirwan, J. P., Jing, M., Presley, L., & Catalano, P. M. (2008) · Diabetes · doi:10.2337/db07-1356 · Cited by 98 · see citing works
Self-citationReversal of Insulin Resistance Postpartum Is Linked to Enhanced Skeletal Muscle Insulin Signaling
Kirwan, J. P., Varastehpour, A., Jing, M. X., Presley, L. H., Shao, J., Friedman, J. E., & Catalano, P. M. (2004) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2004-0749 · Cited by 96 · see citing works
Self-citationSubclinical abnormalities of glucose metabolism in subjects with previous gestational diabetes
Catalano, P. M., Bernstein, I. M., Wolfe, R. R., Srikanta, S., Tyzbir, E. D., & Sims, E. A. H. (1986) · American Journal of Obstetrics and Gynecology · doi:10.1016/0002-9378(86)90155-9 · Cited by 82 · see citing works
Self-citationMechanism of glucose transport across the human and rat placental barrier: A review
Takata, K., & Hirano, H. (1997) · Microscopy Research and Technique · doi:10.1002/(sici)1097-0029(19970701/15)38:1/2 · Cited by 72 · see citing works
Ultrastructural Localization of Insulin Receptors in Human Placenta
Jones, C. J. P., Hartmann, M., Blaschitz, A., & Desoyé, G. (1993) · American Journal of Reproductive Immunology · doi:10.1111/j.1600-0897.1993.tb00614.x · Cited by 43 · see citing works
Molecular phenotype of monocytes at the maternal–fetal interface
Basu, S., Leahy, P. S., Challier, J.-C., Minium, J., Catalano, P., & Mouzon, S. H. (2011) · American Journal of Obstetrics and Gynecology · doi:10.1016/j.ajog.2011.06.037 · Cited by 27 · see citing works
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Flagged first, then by citations
Research works printed but not linked: 1
- [22]22. Desoye G, Hartmann M, Jones CJ, Wolf HJ, Kohnen G, Kosanke G et al. Location of insulin receptors in the placenta and its progenitor tissues. Microsc Res Tech 1997; 38: 36-75.
Cited by
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The Pathophysiology of Gestational Diabetes Mellitus
Plows, J. F., Stanley, J. L., Baker, P. N., Reynolds, C. M., & Vickers, M. H. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19113342 · Cited by 1,874 · see citing works
“The rate of insulin-stimulated glucose uptake is reduced by 54% in GDM when compared with normal pregnancy [84].”
BackgroundBaz, B., Riveline, J.-P., & Gautier, J.-F. (2016) · European Journal of Endocrinology · doi:10.1530/eje-15-0378 · Cited by 260 · see citing works
Treatments for women with gestational diabetes mellitus: an overview of Cochrane systematic reviews
Martis, R., Crowther, C. A., Shepherd, E., Alsweiler, J., Downie, M. R., & Brown, J. (2018) · Cochrane Database of Systematic Reviews · doi:10.1002/14651858.cd012327.pub2 · Cited by 159 · see citing works
Wexler, D. J., Powe, C. E., Barbour, L. A., Buchanan, T., Coustan, D. R., Corcoy, R., Damm, P., Dunne, F., Feig, D. S., Ferrara, A., et al. (2018) · Obstetrics & Gynecology · doi:10.1097/aog.0000000000002726 · Cited by 80 · see citing works
Self-citationHealthy dietary patterns and common pregnancy complications: A prospective and longitudinal study
Li, M., Grewal, J., Hinkle, S. N., Yisahak, S. F., Grobman, W. A., Newman, R. B., Skupski, D. W., Chien, E. K., Wing, D. A., Grantz, K. L., et al. (2021) · The American Journal of Clinical Nutrition · doi:10.1093/ajcn/nqab145 · Cited by 76 · see citing works
Mitanchez, D., Ciangura, C., & Jacqueminet, S. (2020) · Nutrients · doi:10.3390/nu12020353 · Cited by 37 · see citing works
Kondracki, A. J., Valente, M. J., Ibrahimou, B., & Bursac, Z. (2022) · Paediatric and Perinatal Epidemiology · doi:10.1111/ppe.12809 · Cited by 34 · see citing works
Benhalima, K., Van Crombrugge, P., Moyson, C., Verhaeghe, J., Vandeginste, S., Verlaenen, H., Vercammen, C., Maes, T., Dufraimont, E., De Block, C., et al. (2019) · Journal of Clinical Medicine · doi:10.3390/jcm8030383 · Cited by 33 · see citing works
Adverse maternal and neonatal outcomes in pregnant women with abnormal glucose metabolism
Li, M.-F., Ma, L., Yu, T.-P., Zhu, Y., Chen, M.-Y., Liu, Y., & Li, L.-X. (2020) · Diabetes Research and Clinical Practice · doi:10.1016/j.diabres.2020.108085 · Cited by 31 · see citing works
Defective Visceral Adipose Tissue Adaptation in Gestational Diabetes Mellitus
McElwain, C. J., Manna, S., Musumeci, A., Sylvester, I., Rouchon, C., O'Callaghan, A. M., Ebad, M. A. B., McCarthy, F. P., & McCarthy, C. M. (2024) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgad699 · Cited by 7 · see citing works
Diagnosis of gestational diabetes: Evidence and pitfalls
Wong, T., Immanuel, J., Wong, V. W., Barnes, R., & Simmons, D. (2025) · Best Practice & Research Clinical Endocrinology & Metabolism · doi:10.1016/j.beem.2025.102069 · Cited by 4 · see citing works
- Authors
- Catalano, P. M.
- Affiliations
- MetroHealth (US)
- Corresponding author
- Catalano, P. M.
- Venue
- Diabetic Medicine
- Publisher
- Wiley
- Published
- 2014-02-16
- Volume
- 31
- Issue
- 3
- Pages
- 273-281
- ISSN
- 0742-3071 (ISSN-L)
- 1464-5491
- PMC
- PMC4178541
- OpenAlex
- W2164166774
- Cited by
- 456
- References
- 24
- Citations by year
- 2026: 31 · 2025: 45 · 2024: 37 · 2023: 57 · 2022: 70 · 2021: 61 · 2020: 48 · 2019: 31 · 2018: 23 · 2017: 15 · 2016: 19 · 2015: 12 · 2014: 7
- FWCI
- 14.21
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetic Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Child Health and Human Development (HD 22965-19)
- Topics
- Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Keywords
- gestational diabetes mellitus, insulin resistance, insulin sensitivity, IRS-1, insulin receptor tyrosine phosphorylation, hepatic glucose production, skeletal muscle glucose uptake, gestational weight gain, inflammation, TNF-α, placental gene expression, lipid metabolism
- MeSH terms
- Biological Transport, Female, Glucose, Humans, Hyperglycemia, Infant, Newborn, Inflammation, Insulin, Insulin Resistance, Obesity, Phosphorylation, Pregnancy, Prenatal Care, Receptor, Insulin, Signal Transduction, Diabetes, Gestational, Muscle, Skeletal, Receptor Protein-Tyrosine Kinases, Risk Reduction Behavior, Postpartum Period
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