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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #187378
Title: ANEMIA IN CU-DEFICIENT RATS WAS NOT REVERSED BY ADMINISTERING HIGH AMOUNTS OF CU-FREE FE, EITHER PARENTERALLY OR BY DIET

Author
item Reeves, Phillip
item Demars, Lana

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 11/10/2005
Publication Date: 3/6/2006
Citation: Reeves, P.G., DeMars, L.C. 2006. Anemia in Cu-deficient rats was not reversed by administering high amounts of Cu-free Fe, either parenterally or by diet [abstract]. Journal of Federation of American Societies for Experimental Biology. 20(4):A193.

Interpretive Summary:

Technical Abstract: In rats, dietary Cu deficiency (CuD) reduces Fe absorption and leads to anemia (J.Nutr., 134: 1953, 2004) that can be reversed by dietary Cu supplements (Exp. Biol. Med. 230: 320, 2005). Fe supplements reversed anemia in CuD mice (J.Nutr., 114: 422, 1984) and rats (Blood, 34: 747, 1969) but not swine (Blood, 11: 143, 1956). To further assess these effects in rats, two groups of 24 males of weanling age were fed an AIN-93G diet with either low Cu (<0.3 mg/kg) or with adequate Cu (CuA; 5.0 mg/kg). At d-14, 8 rats from each group were fed a similar diet containing 110 mg Fe/kg as Cu-free ferric citrate. Another 8 rats from each group received daily IP injections of 2.5 mg Fe/kg BW as Cu-free ferric citrate. The remaining rats received no Fe supplement. At d-21, all rats were given an oral dose of 59Fe incorporated into 1.0 g of diet. At d-28, blood and tissues were collected to determine Cu and Fe status and 59Fe retention. Signs of CuD, including reduced serum ceruloplasmin activity, anemia, low serum Fe, and low serum and liver Cu, were evident in rats fed the CuD diet. Fe supplementations either by diet or injections did not elevate serum Fe or reverse anemia in the CuD rats. However, when compared with CuA controls, liver Fe was elevated 3-fold in CuD rats without an Fe supplement and 6-fold in CuD rats receiving Fe IP. Compared with the respective CuA controls, the percent of the 59Fe dose retained was reduced in CuD rats with either no Fe supplement or a dietary Fe supplement, but was not affected by receiving Fe IP. These findings suggest that the cause of anemia in CuD rats is a combination of reduced Fe absorption and a failure of Fe utilization for hemoglobin synthesis.