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Effect of increasing iron supplementation on blood lipids in rats

Published online by Cambridge University Press:  09 March 2007

Paul Whittaker*
Affiliation:
Center for Food Safety and Applied Nutrition, Food and Drug Administration, 200 C Street S.W., HFS-236, Washington, DC 20204, USA
Ronald F. Chanderbhan
Affiliation:
Center for Food Safety and Applied Nutrition, Food and Drug Administration, 200 C Street S.W., HFS-236, Washington, DC 20204, USA
*
*Corresponding author: Dr Paul Whittaker, fax +1 202 260 7036, email paul.whittaker@cfsan.fda.gov
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Abstract

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The effects of increasing levels of Fe on serum fatty acids, cholesterol, triacylglycerol, liver and heart were examined in male Sprague–Dawley rats fed either Fe-deficient or carbonyl Fe-supplemented diets with 35 (control), 350, 3500 and 20 000 μg Fe/g for 12 weeks. As intake of Fe increased, serum total cholesterol increased from 2·0 mmol/l in controls to 5·2 mmol/l at the highest level of Fe. Also, the total serum phospholipid fatty acids increased from 609 mg/dl in controls to 1292 mg/l at the highest level of Fe. Except for the highest dose of Fe, the ratio of saturated to unsaturated phospholipid fatty acids increased from 1·2 to 1·7. The serum total free fatty acid levels remained constant among all groups with a range from 162 to 228 mg/l, while a ratio of 0·6 to 0·8 for saturated to unsaturated fatty acids was maintained. A dose-related increase in liver non-haem Fe from 18 to 3500 μg/g correlated with increases in lipid peroxidation (r 0·87), measured by the lipid-conjugated diene assay. Oxidative changes in the liver may have resulted in alterations in sterol synthesis, leading to increased serum cholesterol levels with increases in serum phospholipids and changes in the ratios of their saturated to unsaturated fatty acids. Animals with heart damage showed myocardial degeneration and cardiomyopathy with haemosiderin in interstitial macrophages or myocardial fibres and, when these were coupled with the findings of increased non-haem Fe in the heart and lipid peroxidation in the liver, suggested that oxidative stress is involved in the pathogenesis of the lesions.

Type
Research Article
Copyright
Copyright © The Nutrition Society 2001

Footnotes

The studies reported herein were conducted according to the principles set forth in the Guide for the Care and Use of Laboratory Animals, Institute of Laboratory Animal Resources, National Research Council, National Academy Press, Washington, DC, 1996. The mention of trade names, commercial products, or organizations does not imply endorsement by the US Food and Drug Administration.

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