Submitted to: Trace Elements in Man and Animals (TEMA)
Publication Type: Abstract Only
Publication Acceptance Date: May 2, 1999
Publication Date: N/A
Technical Abstract: The hypothesis that nonenzymatic glycosylation of proteins (glycation) contributes to damage associated with dietary copper (Cu) deficiency has depended largely on indirect evidence. Observation of an elevated percentage of glycated hemoglobin in Cu-deficient rats has thus far provided the only direct evidence of an increase in glycation. We sought further direct evidence of increased glycation in Cu-deficiency. Male weanling rats were fed a Cu-adequate (CuA, 6.4 mg Cu/kg diet) or Cu- deficient diet (CuD, 0.4 mg Cu/kg diet) for five weeks. Rats fed CuD diet were Cu-deficient as judged by depressed organ Cu concentrations as well as several indirect indices (See table). Measurements of hemoglobin A1 and serum fructosamine (both early glycation end-products) as well as serum pentosidine (an advanced glycation end-product) indicated that all three compounds were elevated in CuD relative to CuA rats. This finding further supports the hypothesis that glycation is enhanced and thus may contribute to defects associated with dietary Cu deficiency. Variable <p>CuA <p>CuD Body weight (g) 290+/-7 (28) 256+/-4(28) Heart/body weight ratio (mg/g) 3.46+/-0.05 (28) 5.55+/-0.17 (28) Hematocrit 0.407+/-0.005 (27) 0.203+/-0.008(25) Liver Cu (nmol/g dry weight) 261+/-15(28) 61 +/- 9(28) Hemoglobin A1 (%) 2.07+/-0.03(28) 3.32+/-0.08 (28) Serum fructosamine (nmol/mg protein)21.7+/-0.4 (25) 27.3+/-0.8 (27) Serum pentosidine (pmol/mg protein) ND (17) 6.37+/-1.1(18) Values are means # SEM (n). Value for each characteristic from CuD rats is different from that for the same characteristic in CuA rats (p<0.05).