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Review
. 2012 Oct 10;10:119.
doi: 10.1186/1741-7015-10-119.

Dietary Iron Intake, Body Iron Stores, and the Risk of Type 2 Diabetes: A Systematic Review and Meta-Analysis

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Free PMC article
Review

Dietary Iron Intake, Body Iron Stores, and the Risk of Type 2 Diabetes: A Systematic Review and Meta-Analysis

Wei Bao et al. BMC Med. .
Free PMC article

Abstract

Background: Excess iron has been shown to induce diabetes in animal models. However, the results from human epidemiologic studies linking body iron stores and iron intake to the risk of type 2 diabetes mellitus (T2DM) are conflicting. In this study, we aimed to systematically evaluate the available evidence for associations between iron intake, body iron stores, and the risk of T2DM.

Methods: A systematic search of the PubMed/MEDLINE and EMBASE databases to the end of 22 April 2012 was performed, and reference lists of retrieved articles were screened. Two reviewers independently evaluated the eligibility of inclusion and extracted the data. Pooled relative risks (RRs) and 95% confidence intervals (CIs) were calculated using random-effects models.

Results: We reviewed 449 potentially relevant articles, and 11 prospective studies were included in the analysis. A meta-analysis of five studies gave a pooled RR for T2DM of 1.33 (95% CI 1.19 to 1.48; P<0.001) in individuals with the highest level of heme iron intake, compared with those with the lowest level. The pooled RR for T2DM for a daily increment of 1 mg of heme iron intake was 1.16 (1.09 to 1.23, P<0.001). Body iron stores, as measured by ferritin, soluble transferrin receptor (sTfR) and the sTfR:ferritin ratio, were significantly associated with the risk of T2DM. The pooled RRs for T2DM in individuals with the highest versus the lowest intake of ferritin levels was 1.70 (1.27-2.27, P<0.001) before adjustment for inflammatory markers and 1.63 (1.03-2.56, P = 0.036) after adjustment. We did not find any significant association of dietary intakes of total iron, non-heme, or supplemental iron intake with T2DM risk.

Conclusion: Higher heme iron intake and increased body iron stores were significantly associated with a greater risk of T2DM. Dietary total iron, non-heme iron, or supplemental iron intakes were not significantly associated with T2DM risk.

Figures

Figure 1
Figure 1
Flow chart for study selection (through April 22, 2012).
Figure 2
Figure 2
Associations between dietary total iron, heme iron intake and risk of type 2 diabetes mellitus (T2DM) in the included studies, comparing the highest category with the lowest. The risk estimate of dietary total iron intake for T2DM risk in the Iowa Women's Health Study (Lee et al [24]) was not directly reported, and thus this was pooled from the results of dietary non-heme iron intake and heme iron intake in this study. M, men; W, women.
Figure 3
Figure 3
Dose-response analyses of dietary intakes of total iron and heme iron in relation to risk of type 2 diabetes mellitus (T2DM) in the included studies. The risk estimate of dietary total iron intake for T2DM risk in the Iowa Women's Health Study (Lee et al [24])) was not directly reported, and thus this was pooled from the results of dietary non-heme iron intake and heme iron intake in this study. W, women.
Figure 4
Figure 4
Associations between circulating ferritin levels and risk of type 2 diabetes mellitus (T2DM) in the included studies. M indicates men and W for women. The data in the EPIC-Norfolk study [11] were the results of an ad hoc analysis by the original authors, which used quintiles of ferritin levels as exposure and separately reported for men and women. M, men; W, women.

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References

    1. Andrews NC. Disorders of iron metabolism. N Engl J Med. 1999;341(26):1986–1995. doi: 10.1056/NEJM199912233412607. - DOI - PubMed
    1. Rajpathak SN, Crandall JP, Wylie-Rosett J, Kabat GC, Rohan TE, Hu FB. The role of iron in type 2 diabetes in humans. Biochim Biophys Acta. 2009;1790(7):671–681. doi: 10.1016/j.bbagen.2008.04.005. - DOI - PubMed
    1. Tiedge M, Lortz S, Drinkgern J, Lenzen S. Relation between antioxidant enzyme gene expression and antioxidative defense status of insulin-producing cells. Diabetes. 1997;46(11):1733–1742. doi: 10.2337/diabetes.46.11.1733. - DOI - PubMed
    1. Awai M, Narasaki M, Yamanoi Y, Seno S. Induction of diabetes in animals by parenteral administration of ferric nitrilotriacetate. A model of experimental hemochromatosis. Am J Pathol. 1979;95(3):663–673. - PMC - PubMed
    1. Cooksey RC, Jones D, Gabrielsen S, Huang J, Simcox JA, Luo B, Soesanto Y, Rienhoff H, Abel ED, McClain DA. Dietary iron restriction or iron chelation protects from diabetes and loss of beta-cell function in the obese (ob/ob lep-/-) mouse. Am J Physiol Endocrinol Metab. 2010;298(6):E1236–1243. doi: 10.1152/ajpendo.00022.2010. - DOI - PMC - PubMed
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