Copper Deficiency Reduces Iron Absorption and Biological Half-Life in Male Rats

• Published in: The Journal of nutrition Vol. 134; no. 8; pp. 1953 - 1957
• Main Authors: Reeves, Philip G., DeMars, Lana C.S.
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Elsevier Inc 01.08.2004; American Society for Nutritional Sciences
• Subjects: absorption; animal models; Animals; Biological and medical sciences; biological half-life; Body Weight; copper; Copper - deficiency; Diet; diet-related diseases; erythrocyte count; Feeding. Feeding behavior; Fundamental and applied biological sciences. Psychology; gender differences; Half-Life; hematocrit; hemoglobin; human diseases; Intestinal Absorption; iron; Iron - pharmacokinetics; iron deficiency anemia; isotopes; Male; males; nutrient deficiencies; nutrient retention; nutrient-nutrient interactions; nutritional status; Rats; Rats, Sprague-Dawley; Tissue Distribution; Vertebrates: anatomy and physiology, studies on body, several organs or systems; weanlings; MCV; CuD; RDW; absorption; BHL; biological half-life; copper; iron; WBC; rats; Cp; CuA; Nutrition; Rat; Iron deficiency anemia; Rodentia; Metabolic diseases; Male; Hemopathy; Iron; Inorganic element; Enzymopathy; Micronutrient; Vertebrata; Mammalia; Absorption; Animal; Sideropenia; Copper; Half life
• ISSN: 0022-3166; 1541-6100
• DOI: 10.1093/jn/134.8.1953

Dietary copper deficiency (CuD) in rats leads to iron (Fe) deficiency anemia. Is this because CuD reduces Fe absorption? Fe absorption in CuD rats was determined by feeding diets labeled with 59Fe and using whole-body counting (WBC) to assess the amount retained over time. Two groups, each with 45 male weanling rats, were fed an AIN-93G diet low in Cu (<0.3 mg/kg; CuD) or one containing adequate Cu (5.0 mg/kg; CuA). At intervals over the next 42 d, 5 rats per group were killed and blood was drawn to determine hematocrit, hemoglobin, and other indicators of Fe status. At d 7 and 25, 5 rats per group were fed 1.0 g of their respective diets that had been labeled with 59Fe. Retained 59Fe was monitored for 10 d by WBC; then rats were killed and 59Fe was measured in various organs. Signs of Fe deficiency, such as low hemoglobin, hematocrit, and RBC count, were evident in CuD rats by d 14. At d 7, CuD rats absorbed 90% as much Fe as CuA rats (P > 0.20), but at d 25, CuD rats absorbed only 50% as much as CuA rats (P < 0.001). In the study beginning at d 7, the biological half-life (BHL) of 59Fe in CuD rats was less (P < 0.02) than that in CuA rats [geometric mean (−SEM, +SEM); 75(62,91) d vs. 175(156,195) d]. In the study beginning at d 25, the BHL was again less (P < 0.02) in the CuD rats than in the CuA rats [33(23,49) d for CuD and 157(148,166) d for CuA]. Apparently, the route of Fe loss in the CuD rats was through the gut. At d 16 and 34, CuD rats lost 4 to 5 times more (P < 0.01) 59Fe in the feces in a 24-h period than the CuA rats. Also, 59Fe in the duodenal mucosa of CuD rats was ∼100% higher (P < 0.01) than in CuA rats. These findings suggest that Fe deficiency anemia in CuD male rats is caused at least in part by reductions in Fe absorption and retention.