Original Article
International Journal of Obesity (2007) 31, 1412–1419; doi:10.1038/sj.ijo.0803625; published online 17 April 2007
Inflammation and iron deficiency in the hypoferremia of obesity
L B Yanoff1, C M Menzie1, B Denkinger2,5, N G Sebring2,5, T McHugh3, A T Remaley4,5 and J A Yanovski1,5
- 1Unit on Growth and Obesity, Developmental Endocrinology Branch, National Institute of Child Health and Human Development, Bethesda, MD, USA
- 2Nutrition Department, Hatfield Clinical Research Center, National Institutes of Health, DHHS, Bethesda, MD, USA
- 3Nursing Department, Hatfield Clinical Research Center, National Institutes of Health, DHHS, Bethesda, MD, USA
- 4Department of Laboratory Medicine, Hatfield Clinical Research Center, National Institutes of Health, DHHS, Bethesda, MD, USA
Correspondence: Dr JA Yanovski, Unit on Growth and Obesity, Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Hatfield Clinical Research Center, Room 1E-3330, 10 Center Drive, MSC-1103, Bethesda, MD 20892-1103, USA. E-mail: jy15i@nih.gov
5These authors are Commissioned Officers in the United States Public Health Service, DHHS.
Received 26 November 2006; Revised 23 January 2007; Accepted 21 February 2007; Published online 17 April 2007.
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 86.534.2 g/dl, P=0.002), whereas transferrin receptor (22.67.1 vs 21.07.2 nmol/l, P=0.026), C-reactive protein (0.750.67 vs 0.340.67 mg/dl, P<0.0001) and ferritin (81.188.8 vs 57.688.7 
g/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.
Keywords:
iron deficiency, adiposity, ferritin, inflammation, C-reactive protein, transferrin receptor
MORE ARTICLES LIKE THIS
These links to content published by NPG are automatically generated
RESEARCH
Inhibition of adenyl cyclase by an exotoxin of Bacillus thuringiensis
Nature Letters to Editor (03 Jan 1975)
Inflammation and iron deficiency in the hypoferremia of obesity
International Journal of Obesity Original Article
Capturing the onset of the common cold and its effects on iron absorption
European Journal of Clinical Nutrition Correspondence
Factors determining the percentage of hypochromic red blood cells in hemodialysis patients
Kidney International Original Article
