Hepcidin is the main regulator of systemic iron homeostasis and is primarily produced by the liver but is also expressed, at the mRNA-level, in periphery tissues including the subcutaneous and visceral adipose tissue. Obesity is associated with elevated hepcidin concentrations and iron depletion suggesting that the exaggerated fat mass in obesity could contribute significantly to circulating hepcidin levels consequently altering iron homeostasis. The objective of this study was to determine if abdominal subcutaneous adipose tissue (AbScAT) releases hepcidin in vivo and if release is modified by obesity. Arterio-venous differences in concentrations of hepcidin were measured across AbScAT in 9 obese and 9 lean adults. Overall (n = 18), mean plasma hepcidin concentrations were significantly higher in arterialized compared to AbScAT venous samples [mean difference (arterialized-AbScAT venous plasma hepcidin) = 4.9 ± 9.6 ng/mL, P = 0.04]. Net regional release was not calculated because mean venous plasma hepcidin concentrations were lower than mean arterialized concentrations indicating no net release. Significant correlations between AbScAT venous and arterialized plasma hepcidin concentrations with anthropometric variables were not observed. Findings from this vein drainage study suggest there is no net release of hepcidin from the AbScAT depot and thereby no ability to signal systemically, even in obesity.

Objective

To examine iron metabolism during the second and third trimesters in African American women with high-risk pregnancies.

Design

Longitudinal pilot study.

Setting

Large, university-based, urban Midwestern U.S. medical center.

Participants

Convenience sample of 32 African American women with high-risk pregnancies seeking care at an urban maternal-fetal medicine clinic.

Methods

Nonfasting venous blood was collected in the second and third trimesters to assess iron status, hepcidin, and systemic inflammation. Anthropometric and survey data were obtained via self-report. Descriptive statistics were calculated from these data, and changes in the clinical parameters between the second and third trimesters were evaluated via paired t tests. Associations among demographic, reproductive, anthropometric, inflammatory, and iron-related parameters were also assessed in each trimester.

Results

The mean age of participants was 28.3 (± 6.8) years, and mean prepregnancy body mass index was 31.9 (± 10.7) kg/m². In the longitudinal analysis, significant (p < .05) declines in serum iron, ferritin, transferrin saturation, and C-reactive protein were observed between the second and third trimesters. There was no statistically significant change in hepcidin between trimesters. When using a ferritin level cut-point of less than 15 ng/ml and soluble transferrin receptor level of greater than 28.1 nmol/L, 48% of the participants (14 of 29) were classified with iron deficiency in the third trimester.

Conclusion

In this pilot study, iron deficiency was prevalent among a small cohort of African American women with high-risk pregnancies. Hepcidin concentrations were greater than previously reported in healthy, pregnant, primarily White women, which suggests decreased iron bioavailability in this high-risk group.