Adipokine profiles in preeclampsia

Abstract

Objectives: Hypertensive disorders of pregnancy (HDP), including preeclampsia (PE), are associated with short- and long-term maternal health complications, and obesity is a leading attributable risk factor for HDP. Yet, most women identified as obese [by body mass index (BMI) ≥ 30 kg/m²] do not develop HDP, indicating limited predictability of BMI alone. In nonpregnant populations, increased visceral fat mass (VFM) is an obesity-associated phenotype increasing the risk of developing hypertension. We sought to assess whether, in pregnancy, obese women with PE would have higher circulating levels of adipokines preferential to VFM compared to obese women without PE.

Study Design: We performed a case-control study of women with and without PE, including obese (n = 65; BMI ≥ 30 kg/m²) and normal weight (n = 52; BMI 18.4–24.9 kg/m²) women. Plasma concentrations of adipokines preferential to VFM (visfatin, resistin), adipokines reflecting overall adiposity (leptin, adiponectin), and inflammatory cytokines were compared.

Results: We found that among obese women, cases had significantly higher levels of VFM-associated adipokines and cytokines compared to controls [visfatin (p < .01, t = −3.8), resistin (p = .002, t = 1.12), IFN gamma (p = .04, t = −2.0), IL-6 (p < .01, t = −2.65), IL1-beta (p < .01, t = −4.1), IL-2 (p < .01, t = −3.9)]. Interestingly, however, obese and normal weight cases had similar VFM-adipokine and cytokine levels [visfatin (p = .34, t = −0.35), resistin (p = .55, t = −0.25)], and inflammatory marker concentrations [IFN gamma (p = .86, t = −0.76), IL-6 (p = .91, t = −0.53), IL-1beta (p = .67, t = 1.18), and IL-2 (p = .45, t = −1.16)]. These data possibly suggest an association between VFM and PE that is present independent of BMI.

Conclusion: In summary, we demonstrated that, in normal-weight and obese women, PE was associated with higher concentrations of VFM-preferential adipokines compared to normal-weight and obese controls without PE.

Keywords:

• Obesity
• preeclampsia
• visceral fat

Acknowledgements

This research was conducted using specimens and data collected and stored on behalf of the Global Alliance to Prevent Prematurity and Stillbirth (GAPPS) Repository Samples were processed through the Fred Hutchinson Cytokine Laboratory (Seattle, WA).

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This work was supported by grants NIH R01 DK 089036 (Ellen A. Schur), NICHD Women’s Reproductive Health Research (WRHR) Grant K12 HD001264-17 (Suchitra Chandrasekaran), and K08HD067221 (Hilary Gammill).