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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Healthy Body Weight Research » Research » Publications at this Location » Publication #127874


item Klevay, Leslie

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: 12/1/2001
Publication Date: 3/20/2002
Citation: Klevay, L.M. 2002. Copper deficiency increases serum amyloid A in adult mice [abstract]. Federation of American Societies for Experimental Biology Journal. 16:A374.

Interpretive Summary:

Technical Abstract: Associations among lipid metabolism, atherosclerosis and ischemic heart disease (IHD) are well known; a similar, weaker association of inflammation with these pathologies is more recently recognized. In view of numerous anatomical, chemical and physiological similarities between animals deficient in copper and people with IHD, the hypothesis that copper deficiency can alter some acute phase proteins was tested. Thirty-two male mice of the Swiss Webster strain were matched into 2 groups of 16 by mean weight (29g). They were given a purified diet (Klevay, Atherosclerosis 54:213, 1985) based on sucrose (58%), lard (28%) and casein (8%). Half the mice received a drinking solution containing Cu, I, Mn and Zn and half the latter 3 elements alone (loc. cit.). After 46 days without aqueous copper, dry liver copper was decreased (mean +/- SE) (2.9 +/- 0.3 vs 4.3 +/- 0.2 ug/g, t=3.79, p=0.0009) and serum amyloid A was increased from 18 +/- 1.8 to 35 +/- 7.2 ug/ml, (t=2.4, p<0.03). Plasma cholesterol was elevated insignificantly, but heart weight increased by 30% (p=0.0001). Interlukin-6 was unchanged (<1%). Proteins were measured by ELISA. Amyloid increase in human heart disease and in copper deficiency may occur because of lipoprotein properties instead of inflammatory properties.