Objective We investigated the relationships of maternal circulating individual free fatty acids (FFA) with insulin resistance, insulin secretion and inflammatory biomarkers during mid-pregnancy.
Research design and methods The data were drawn from a prospective cohort of generally healthy pregnant women (n=1368, African-American 36%, Hispanic 48%, Caucasian 16%) in Camden, NJ. We quantitatively determined 11 FFAs, seven cytokine/adipokine, homeostatic model assessment of insulin resistance (HOMA-IR) and C-peptide levels from the fasting blood samples that were collected at 16 weeks of gestation. Multivariate analyses were performed along with separate analyses for each individual FFA.
Results High HOMA-IR (p<0.001) and C-peptide (p<0.0001) levels were positively associated with a twofold to fourfold increased risk for developing gestational diabetes mellitus (GDM). Negative relationships were found with specific FFAs (molecular percentage, palmitoleic, oleic, linolenic, myristic acids) and HOMA-IR and C-peptide levels (p<0.01 to p<0.0001). In contrast, palmitic, stearic, arachidonic, dihomo-γ-linolenic (DGLA) and docosahexaenoic acids were positively associated with HOMA-IR and C-peptide (p<0.01 to p<0.0001). The individual FFAs also predicted cytokine/adipokine levels. For example, women who had elevated DGLA (highest quartile) were twice as (adjusted OR 2.06, 95% CI 1.42 to 2.98) likely to have higher interleukin (IL)-8 (p<0.0001) levels. Conversely, women with high palmitoleic, oleic, and linolenic acid levels had reduced odds (≥2-fold, p<0.01 to p<0.001) for having higher IL-8, IL-6 or tumor necrosis factor-alpha levels.
Conclusion Our results suggest that maternal individual FFAs uniquely affect insulin resistance and secretion. The effects are either direct or indirect via modulation of the inflammatory response. Modifying the composition of FFAs may help in reducing the risk of GDM.
- free fatty acid(s)
- insulin resistance
- gestational diabetes mellitus
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Presented at Part of data from this study was presented in abstract form at the American Diabetes Association (ADA) 78th Scientific Sessions, Orlando, FL, 22–26 June 2018.
Contributors XC designed the study, obtained funding and wrote the manuscript. TPS contributed to the laboratory method(s) and the quality of the free fatty acid measurements. RAS contributed to overseeing the statistical analyses of the data. TOS contributed to the design and obtained funding for the prospective cohort study. All authors participated in the interpretation of data and the writing, reviewing, editing of the manuscript and had the final responsibility for approving the submitted version of the manuscript. XC is the guarantor of this work and, as such, had full access to all data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Funding This research was supported by the National Institute on Minority Health and Health Disparities grant (R01-MD007828 to XC) and the National Institute of Child Health and Human Development grant (HD038329 to TOS).
Competing interests None declared.
Patient consent for publication Not required.
Ethics approval The institutional review board at the University of Medicine and Dentistry of New Jersey (which later became Rowan University School of Osteopathic Medicine in 2013) approved the study’s protocol.
Provenance and peer review Not commissioned; externally peer reviewed.
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