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Cited by 105Gestational Diabetes Research and ManagementDiabetes, Cardiovascular Risks, and LipoproteinsPancreatic function and diabetes

The DOI matches its Crossref record; 47 of the 48 references it cites were found in a registry or an index.

Free fatty acids, insulin resistance, and pregnancy

Sivan, Eyal, Boden, Guenther·2003·Current Diabetes Reports
DOI 10.1007/s11892-003-0024-y
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Abstract

Acute elevation of plasma free fatty acid (FFA) levels causes insulin resistance to rise dose dependently in pregnant and nonpregnant women. Plasma FFA levels are commonly elevated during late pregnancy, partly due to rising blood levels of lipolytic placental hormones, and are a likely cause for much of the increase in insulin resistance occurring at that time in all pregnant women. Plasma FFA levels are similar or higher and the insulin resistance is comparable or more severe in women with gestational diabetes mellitus (GDM) than in nondiabetic pregnant women. In contrast to healthy pregnant women, insulin secretion in women with GDM is defective and, therefore, is unable to rise adequately to compensate for the insulin resistance; the result is hyperglycemia. The mechanism by which elevated plasma FFA levels cause insulin resistance in skeletal muscle includes intramyocellular accumulation of diacylglycerol, which activates protein kinase C (the b II and d isoforms). This results in reduction of tyrosine phosphorylation of the insulin receptor substrate-1 and inhibits activation of phosphoinositol-3 kinase, an enzyme that is essential for normal insulin-stimulated glucose uptake.

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Crossref · 10.1007/s11892-003-0024-y

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47 of 47 references verified0 citation errors · 0 not checkable

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Citations

Cites

Research works printed but not linked: 1

  1. Buchanan TA, Catalano PM: The pathogenesis of GDM: implication for diabetes after pregnancy. Diabetes 1995, 3:584–601.

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Metadata

Authors
Sivan, E., & Boden, G.
Affiliations
Temple University Hospital (US)
ORCID
Sivan, Eyal
Venue
Current Diabetes Reports
Publisher
Springer Science and Business Media LLC
Published
2003-07
Volume
3
Issue
4
Pages
319-322
ISSN
  • 1534-4827 (ISSN-L)
  • 1539-0829
DOI
10.1007/s11892-003-0024-y
OpenAlex
W2139126524
Cited by
105
References
48
Citations by year
2026: 6 · 2025: 5 · 2024: 4 · 2023: 6 · 2022: 9 · 2021: 8 · 2020: 5 · 2019: 5 · 2018: 9 · 2017: 5 · 2016: 6 · 2015: 1 · 2014: 5 · 2013: 4 · 2012: 5
FWCI
0.91
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Current Diabetes Reports (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • American Diabetes Association
  • National Institutes of Health (5r01ag015363-05)
  • National Institute on Aging (AG15363)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK58895, R01DK058895)
  • National Center for Research Resources (M01RR000349, 2 M01 RR00349)
  • NIH Clinical Center
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 › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
Keywords
free fatty acids, insulin resistance, pregnancy, gestational diabetes mellitus, insulin secretion, skeletal muscle, diacylglycerol, protein kinase C, IRS-1, phosphatidylinositol 3-kinase, insulin-stimulated glucose uptake, hyperglycemia
MeSH terms
Fatty Acids, Nonesterified, Female, Humans, Insulin, Insulin Resistance, Pregnancy, Diabetes, Gestational, Carbohydrate Metabolism, Lipid Metabolism

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