Inflammation and iron deficiency in the hypoferremia of obesity

Abstract

Context: Obesity is associated with hypoferremia, but it is unclear if this condition is caused by insufficient iron stores or diminished iron availability related to inflammation-induced iron sequestration. Objective: To examine the relationships between obesity, serum iron, measures of iron intake, iron stores and inflammation. We hypothesized that both inflammation-induced sequestration of iron and true iron deficiency were involved in the hypoferremia of obesity. Design: Cross-sectional analysis of factors anticipated to affect serum iron. Setting: Outpatient clinic visits. Patients: Convenience sample of 234 obese and 172 non-obese adults. Main outcome measures: Relationships between serum iron, adiposity, and serum transferrin receptor, C-reactive protein, ferritin, and iron intake analyzed by analysis of covariance and multiple linear regression. Results: Serum iron was lower (75.8±35.2 vs 86.5±34.2 g/dl, P=0.002), whereas transferrin receptor (22.6±7.1 vs 21.0±7.2 nmol/l, P=0.026), C-reactive protein (0.75±0.67 vs 0.34±0.67 mg/dl, Pμg/l, P=0.009) were higher in obese than non-obese subjects. Obese subjects had a higher prevalence of iron deficiency defined by serum iron (24.3%, confidence intervals (CI) 19.3–30.2 vs 15.7%, CI 11.0–21.9%, P=0.03) and transferrin receptor (26.9%, CI 21.6–33.0 vs 15.7%, CI 11.0–21.9%, P=0.0078) but not by ferritin (9.8%, CI 6.6–14.4 vs 9.3%, CI 5.7–14.7%, P=0.99). Transferrin receptor, ferritin and C-reactive protein contributed independently as predictors of serum iron. Conclusions: The hypoferremia of obesity appears to be explained both by true iron deficiency and by inflammatory-mediated functional iron deficiency.