Cited by 71Gestational Diabetes Research and ManagementAdipokines, Inflammation, and Metabolic DiseasesPancreatic function and diabetes

The Role of Adipokines in Gestational Diabetes Mellitus

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Al-Badri, Marwa R., Zantout, Mira S., Azar, Sami T.·2015·Therapeutic Advances in Endocrinology and Metabolism

Abstract

Gestational diabetes mellitus (GDM) is a complication of pregnancy that is characterized by impaired glucose tolerance with onset or first recognition during pregnancy. The reported prevalence of GDM varies between 0.6% and 20% of pregnancies depending on screening method, gestational age and the population studied. GDM is characterized by pancreatic β-cell function that is insufficient to meet the body’s insulin needs. Available evidence suggests that β-cell defects in GDM result from the same spectrum of causes that underline hyperglycemia in general, including autoimmune disease, monogenic causes and insulin resistance. Adipokines are proteins secreted from the adipocytes and are believed to have a metabolic influence. Our review suggests that, in GDM, various adipokines, mainly leptin and adiponectin, are dysregulated. These two adipokines might have both prognostic and pathophysiological significance in this disease.

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Crossref · 10.1177/2042018815577039

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  • GDM-associated biomarkers contribute to the intrauterine conditions that predispose the offspring to long-term metabolic and cardiometabolic disorders.

    “By influencing placental signaling pathways, nutrient transport, and gene expression, GDM-associated biomarkers contribute to the intrauterine conditions that predispose the offspring to long-term metabolic and cardiometabolic disorders [48].”

    From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [48]

    The Introduction (page unavailable) reports that people born to mothers with GDM have a higher risk of obesity and type 2 diabetes as adults. The Methods (page unavailable) describe adipokine-related placental signaling, amino acid uptake, and possible in-utero programming of obesity, but treat the programming mechanism as tentative. They do not establish that GDM-associated biomarkers alter gene expression to cause long-term metabolic or cardiometabolic disorders in offspring. (LLM, conf=0.85)

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Research works printed but not linked: 1

  1. Masuyama H., 2011, Endocrinol J, 58, 47

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Authors
Al-Badri, M. R., Zantout, M. S., & Azar, S. T.
Affiliations
American University of Beirut Medical Center (LB)
Venue
Therapeutic Advances in Endocrinology and Metabolism
Published
2015-03-23
Volume
6
Issue
3
Pages
103-108
ISSN
  • 2042-0188 (ISSN-L)
  • 2042-0196
OpenAlex
W1969858460
Cited by
71
References
22
Citations by year
2026: 3 · 2025: 3 · 2024: 3 · 2023: 5 · 2022: 5 · 2021: 8 · 2020: 6 · 2019: 8 · 2018: 11 · 2017: 11 · 2016: 6 · 2015: 2
FWCI
11.38
Type
journal article
Language
en
Open access
Locations
  • Therapeutic Advances in Endocrinology and Metabolism (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics
  • Health Sciences › Medicine › Obstetrics and Gynecology › Gestational Diabetes Research and Management
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Keywords
gestational diabetes mellitus, adipokines, leptin, adiponectin, beta-cell dysfunction, insulin resistance, impaired glucose tolerance, adipocytes

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