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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 #94921


item Saari, Jack
item Dahlen, Gwen

Submitted to: Journal of Nutritional Biochemistry
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/30/1998
Publication Date: N/A
Citation: N/A

Interpretive Summary: Altered metabolism of sugar, as commonly occurs in diabetes and aging, may increase blood sugar. This can lead to the undesirable binding of sugar to proteins (termed glycation) that causes damage to the proteins and may alter their function. We have shown previously that this altered sugar binding may be the cause of problems associated with dietary copper deficiency. To date, however, the only direct evidence that altered sugar binding occurs in copper deficiency has been the observation of an elevated percentage of sugar bound to the blood protein hemoglobin. The purpose of the present study was to look for stronger evidence of sugar binding by proteins in copper deficiency by measuring the concentration of another protein containing bound sugar as well as a compound that represents protein that has been destroyed by sugar binding. We found that two such compounds were elevated in copper-deficient rats, thus further confirming the occurrence of a harmful enhanced binding of sugar to proteins in dietary copper deficiency.

Technical Abstract: The hypothesis that nonenzymatic glycosylation of proteins (glycation) contributes to damage associated with dietary copper deficiency has depended largely on indirect evidence. Observation of an elevated percentage of glycated hemoglobin in copper-deficient rats has thus far provided the only direct evidence of an increase in glycation. We sought further direct evidence of increased glycation in copper deficiency. Male weanling rats were fed a copper-adequate (CuA, 6.4 mg Cu/kg diet) or copper deficient diet (CuD, 0.4 mg Cu/kg diet) for five weeks. Rats fed CuD diet were copper deficient as judged by depressed organ copper concentrations as well as a variety of indirect indices. 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 view that glycation is enhanced and thus may contribute to defects associated with dietary copper deficiency.