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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 #79318


item Keehr, Kay
item Hunt, Curtiss
item Idso, Joseph

Submitted to: North Dakota Academy of Science Proceedings
Publication Type: Other
Publication Acceptance Date: 9/15/1997
Publication Date: N/A
Citation: N/A

Interpretive Summary: When infants get inadequate amounts of copper from their diet or mothers' milk, their bones do not form properly and the skeleton becomes misshapen. Thus, we performed a study to determine how bones develop when infants receive just a little less than sufficient amounts of copper in their diet or mothers milk. We tested this idea with pregnant rats who were fed a diet adquate in all vitamins and minerals except for copper. One group o pregnant rats was fed sufficient amounts of copper and another group was fed just slightly less than adequate amounts of copper. After birth half of slightly copper-inadequate mothers were given even less copper. When the rat pups were 28 days old, we found that insufficient amounts of copper did not reduce the body weight of the pups. However, the bones from pups whose mothers were fed just slightly less than adequate amounts of copper were not normal; bone development was retarded. However, those rats fed even less amounts (but not extremely low amounts) of copper looked almost normal. We conclude that the mother must experience a relatively large reduction in copper intake during pregnancy and lactation before the infant changes the rate at which it takes in copper, gets rid of copper, or redistributes the copper stored elsewhere in the body.

Technical Abstract: Severely copper-deficient animals and humans exhibit impaired osteogenesis and bone deformities. We examined bone morphology in female weanling rats exposed to an immune challenge, and born to dams who were exposed to marginal and moderate copper deficiency during gestation and lactation. During gestation, dams were fed the basal diet supplemented with cupric carbonate to provide a total of 1.8 mg Cu/kg diet (G1.8) or 6.0 mg Cu/kg (control diet; G6.0) until parturition. During pup lactation, G1.8 dams were either switched to a diet that provided a total of 0.9 mg Cu/kg (L0.9) or maintained on the same diet (L1.8); G6.0 dams remained on the same diet during lactation (L6.0). On day 21, pups were weaned, injected with sheep red blood cells (SRBC) and maintained on their respective lactation diets. The heights of the proliferative , hypertrophic, and calcified zones of the epiphyseal growth plate were determined at four selected sites by standard image analysis. Compared with the control group (G6.0/L6.0/P6.0), the marginal (G1.8/L1.8/P1.8) and the moderate (G1.8/L0.9/P0.9) copper-deficient groups exhibited progressively reduced copper status as indicated by progressive reductions in serum ceruloplasmin concentrations. These results were similar to those reported earlier in rats not challenged with SRBC. Hepatic cytochrome c oxidase activity was lowest in the moderate group. Marginal copper deficiency altered growth plate morphology, with apparent recovery in the G1.8/L0.9/P0.9 group. The findings indicate that bone metabolism is vulnerable to small decreases of copper status, and large decreases of dietary copper are needed to stimulate homeostatic copper control mechanisms to protect the structure of the growing rat bone.