The DOI matches its Crossref record; 88 of the 88 references it cites were found in a registry or an index.
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).
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“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]
The cited source says what the claim attributes to it.
In the citing paper
“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]
In the citing paper
“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]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
1 retracted
Insulin Stimulates PKCζ-mediated Phosphorylation of Insulin Receptor Substrate-1 (IRS-1)
Liu, Y., Paz, K., Herschkovitz, A., Alt, A., Tennenbaum, T., Sampson, S. R., Ohba, M., Kuroki, T., LeRoith, D., & Zick, Y. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m007281200 · Cited by 159
RetractedIncreased oxidative stress in obesity and its impact on metabolic syndrome
Furukawa, S., Fujita, T., Shimabukuro, M., Iwaki, M., Yamada, Y., Nakajima, Y., Nakayama, O., Makishima, M., Matsuda, M., & Shimomura, I. (2004) · Journal of Clinical Investigation · doi:10.1172/jci21625 · Cited by 5,508
Weyer, C., Funahashi, T., Tanaka, S., Hotta, K., Matsuzawa, Y., Pratley, R. E., & Tataranni, P. A. (2001) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.86.5.7463 · Cited by 3,541
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
Elchebly, M., Payette, P., Michaliszyn, E., Cromlish, W., Collins, S., Loy, A. L., Normandin, D., Cheng, A., Himms-Hagen, J., Chan, C.-C., et al. (1999) · Science · doi:10.1126/science.283.5407.1544 · Cited by 2,210
PPARγ Is Required for the Differentiation of Adipose Tissue In Vivo and In Vitro
Rosen, E. D., Sarraf, P., Troy, A. E., Bradwin, G., Moore, K. J., Milstone, D. S., Spiegelman, B. M., & Mortensen, R. M. (1999) · Molecular Cell · doi:10.1016/s1097-2765(00)80211-7 · Cited by 2,081
Absence of S6K1 protects against age- and diet-induced obesity while enhancing insulin sensitivity
Um, S. H., Frigerio, F., Watanabe, M., Picard, F., Joaquin, M., Sticker, M., Fumagalli, S., Allegrini, P. R., Kozma, S. C., Auwerx, J., et al. (2004) · Nature · doi:10.1038/nature02866 · Cited by 1,677
Aguirre, V., Uchida, T., Yenush, L., Davis, R., & White, M. F. (2000) · Journal of Biological Chemistry · doi:10.1074/jbc.275.12.9047 · Cited by 1,487
Tumor Necrosis Factor α: A Key Component of the Obesity-Diabetes Link
Hotamışlıgil, G. S., & Spiegelman, B. M. (1994) · Diabetes · doi:10.2337/diab.43.11.1271 · Cited by 1,353
Schoonjans, K., Peinado‐Onsurbe, J., Lefebvre, A. M., Heyman, R. A., Briggs, M., Deeb, S., Staels, B., & Auwerx, J. (1996) · The EMBO Journal · doi:10.1002/j.1460-2075.1996.tb00918.x · Cited by 1,173
Flagged first, then by citations
Cited by
Sorted by citations
Host Remodeling of the Gut Microbiome and Metabolic Changes during Pregnancy
Koren, O., Goodrich, J. K., Cullender, T. C., Spor, A., Laitinen, K., Kling Bäckhed, H., Gonzalez, A., Werner, J. J., Angenent, L. T., Knight, R., et al. (2012) · Cell · doi:10.1016/j.cell.2012.07.008 · Cited by 2,165
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
Trends in insulin resistance: insights into mechanisms and therapeutic strategy
Li, M., Chi, X., Wang, Y., Setrerrahmane, S., Xie, W., & Xu, H. (2022) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-022-01073-0 · Cited by 939
A Clinical Update on Gestational Diabetes Mellitus
Sweeting, A., Wong, J., Murphy, H. R., & Ross, G. P. (2022) · Endocrine Reviews · doi:10.1210/endrev/bnac003 · Cited by 928
Application of exosomes as liquid biopsy in clinical diagnosis
Zhou, B., Xu, K., Zheng, X., Chen, T., Wang, J., Song, Y., Shao, Y., & Zheng, S. (2020) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-020-00258-9 · Cited by 685
Metadata
- 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 › Endocrinology, Diabetes and Metabolism › 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
