• Hoi Lun Cheng, Christian E Bryant, Kieron B Rooney, Katharine S Steinbeck, Hayley J Griffin, Peter Petocz, and Helen T O'Connor.
• Discipline of Exercise and Sport Science, Faculty of Health Sciences, The University of Sydney, Sydney, New South Wales, Australia. hche3056@uni.sydney.edu.au
• Plos One. 2013 Jan 1; 8 (7): e68675.

Background And AimsEvidence suggests obesity-related inflammation alters iron metabolism potentially increasing the risk of iron deficiency. This cross-sectional study aimed to investigate iron, hepcidin and inflammatory status in young, healthy overweight and obese women.Methods114 young (18-25 years), healthy comorbidity-free women with a body mass index (BMI) ≥27.5 kg/m(2) were recruited. Biochemical data were analysed using mean ± standard deviation or median (interquartile range) and multivariate modelling. Biochemical markers were also stratified according to varying degrees of overweight and obesity.ResultsAnaemia (haemoglobin <120 g/l) and iron deficiency (serum ferritin <15.0 µg/l) were prevalent in 10% and 17% of participants respectively. Mean/median soluble transferrin receptor was 1.61±0.44 mg/l; hepcidin 6.40 (7.85) ng/ml and C-reactive protein (CRP) 3.58 (5.81) mg/l. Multivariate modelling showed that BMI was a significant predictor of serum iron (coefficient = -0.379; standard error = 0.139; p = 0.008), transferrin saturation (coefficient = -0.588; standard error = 0.222; p = 0.009) and CRP (coefficient = 0.127; standard error = 0.024; p<0.001). Stratification of participants according to BMI showed those with ≥35.0 kg/m(2) had significantly higher CRP (p<0.001) than those in lower BMI categories.ConclusionsIncreasing obesity was associated with minor disturbances in iron metabolism. However, overall outcomes indicated simple iron deficiency (hypoferritinaemia) was the primary iron-related abnormality with no apparent contribution of inflammation or hepcidin, even in those with BMI >35.0 kg/m(2). This indicates that obesity alone may not be sufficient to induce clinically significant disturbances to iron metabolism as previously described. This may be attributed to the lack of comorbidity in this cohort.

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