Cellular Mechanisms for Insulin Resistance in Normal Pregnancy and Gestational Diabetes
Open accessAbstract
The incidence of gestational diabetes mellitus (GDM) has doubled over the last 6–8 years and is paralleling the obesity epidemic. GDM carries longterm implications for the subsequent development of type 2 diabetes in the mother and increased risk for obesity and glucose intolerance in the offspring. Insulin resistance exists before pregnancy in women with a history of GDM but worsens during gestation. Insulin secretion is inadequate to compensate for the insulin resistance, leading to hyperglycemia that is detected by routine glucose screening in pregnancy. Thus, chronic insulin resistance is a central component of the pathophysiology of GDM. Human pregnancy is characterized by a series of metabolic changes that promote adipose tissue accretion in early gestation, followed by insulin resistance and facilitated lipolysis in late pregnancy. In early pregnancy, insulin secretion increases, while insulin sensitivity is unchanged, decreased, or may even increase (1,2). However, in late gestation, maternal adipose tissue depots decline, while postprandial free fatty acid (FFA) levels increase and insulin-mediated glucose disposal worsens by 40–60 % compared with prepregnancy (2).
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Pro-inflammatory cytokines induce insulin resistance by diminishing insulin receptor tyrosine kinase activity, increasing serine phosphorylation of IRS-1, or through the STAT3-SOCS3 pathway, which degrades IRS-1.
“These factors induce insulin resistance either by diminishing insulin receptor (IR) tyrosine kinase activity, increasing serine phosphorylation of IRS-1, or through the STAT3-SOCS3 pathway, which degrades IRS-1 [85,116].”
From The Pathophysiology of Gestational Diabetes Mellitus (2018) · cites this paper as [85]
The section on placental hormones and adipokines (page unavailable) says TNF-α increases IRS-1 serine phosphorylation and diminishes insulin receptor tyrosine kinase activity. The IRS-1 serine phosphorylation section discusses IRS-1 degradation through p70 S6K activation, but does not identify a STAT3–SOCS3 pathway; that attributed mechanism is unsupported by our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn the Barbour study, a 1.5-2-fold increase in the level of the p85α PI-3-kinase regulatory subunit was found in both muscle and adipose tissue of obese pregnant and pregnant GDM women compared to obese non-pregnant women.
“In the Barbour study, a 1.5–2-fold increase in the level of the p85α PI-3-kinase regulatory subunit was found in both the muscle and adipose tissue of obese pregnant and pregnant GDM women compared to obese non-pregnant women.”
From Gestational Diabetes Mellitus—Recent Literature Review (2022) · cites this paper as [43]
The “Increased p85 monomer of PI 3-kinase” section (page unavailable) reports higher p85α levels in both skeletal muscle and adipose tissue from pregnant and GDM subjects than from obese nonpregnant women. It specifies a 1.5–2.0-fold increase for obese pregnant women, but does not explicitly give that magnitude for the GDM group. (LLM, conf=0.88)
Experimental — accuracy not yet measuredReduced tyrosine or increased serine/threonine phosphorylation of the insulin receptor dampens insulin signaling in GDM.
“While insulin receptor abundance is usually unaffected, reduced tyrosine or increased serine/threonine phosphorylation of the insulin receptor dampens insulin signaling [85].”
From The Pathophysiology of Gestational Diabetes Mellitus (2018) · cites this paper as [85]
In women with GDM, a 62% increase in phosphorylation activity of IRS-1 serine residues was found in striated muscle cells compared with control pregnant women without GDM.
“In women with GDM, a 62% increase in the phosphorylation activity of IRS-1 serine residues was found in striated muscle cells compared with the control group of pregnant women without GDM, which points to insulin resistance post-receptor mechanisms [43].”
From Gestational Diabetes Mellitus—Recent Literature Review (2022) · cites this paper as [43]
Pregnancy is characterized by metabolic changes promoting adipose tissue growth during the early phase, followed by an insulin resistance state with its peak during the third trimester.
“This is because pregnancy condition is characterized by a series of metabolic changes promoting adipose tissue growth during the early phase, which is followed by an IR state with its peak during the 3rd trimester [56, 57].”
From From Prediabetes to Type 2 Diabetes Mellitus in Women with Polycystic Ovary Syndrome: Lifestyle and Pharmacological Management (2020) · cites this paper as [57]
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Yao, Y., Cai, X. T., Chen, C., Fang, H., Zhao, Y., Fei, W., Chen, F., & Zheng, C. (2020) · Frontiers in Pharmacology · doi:10.3389/fphar.2020.00643 · Cited by 62 · see citing works
Epigenetic Changes in Gestational Diabetes Mellitus
Dłuski, D. F., Wolińska, E., & Skrzypczak, M. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22147649 · Cited by 68 · see citing works
Beta-cell compensation and gestational diabetes
Usman, T. O., Chhetri, G., Yeh, H., & Dong, H. H. (2023) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2023.105405 · Cited by 72 · see citing works
- Authors
- Barbour, L. A., McCurdy, C. E., Hernandez, T. L., Kirwan, J. P., Catalano, P. M., & Friedman, J. E.
- Affiliations
- University of Colorado Health (US)
- MetroHealth Medical Center (US)
- ORCID
- Venue
- Diabetes Care
- Publisher
- American Diabetes Association
- Published
- 2007-07-01
- Volume
- 30
- Issue
- Supplement_2
- Pages
- S112-S119
- ISSN
- 0149-5992 (ISSN-L)
- 1935-5548
- OpenAlex
- W2079577144
- Cited by
- 811
- References
- 88
- Citations by year
- 2026: 48 · 2025: 43 · 2024: 53 · 2023: 58 · 2022: 77 · 2021: 76 · 2020: 70 · 2019: 63 · 2018: 57 · 2017: 40 · 2016: 51 · 2015: 30 · 2014: 40 · 2013: 24 · 2012: 15
- FWCI
- 18.78
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes Care (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5f32dk075252-02)
- U.S. Public Health Service (MDIRR000051)
- National Institute of Diabetes and Digestive and Kidney Diseases (F32-DK-075252, K23-DK17496, P30DK048520, DK-62115)
- National Center for Research Resources (RR 00080)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HD11089, R01HD022965)
- Topics
- Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- insulin resistance, gestational diabetes mellitus, pregnancy, type 2 diabetes risk, adipose tissue, lipolysis, free fatty acids, insulin secretion, glucose disposal, maternal obesity
- MeSH terms
- Female, Glucose, Hormones, Humans, Insulin Resistance, Placenta, Pregnancy, Reference Values, Diabetes, Gestational, Muscle, Skeletal
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