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Is decreased activity of C-II activated lipoprotein lipase in type III hyperlipoproteinemia (broad-β-disease) a cause or an effect of increased apolipoprotein E levels?
Authors:D Ganesan  H B Bass  W J McConathy  P Alaupovic
Abstract:Apolipoprotein E (ApoE; "arginine-rich" polypeptide) strongly inhibited both C-I and C-II activated lipoprotein lipases but not the protamine insensitive triglyceride lipase. Inhibition of lipoprotein lipases by ApoE in contrast to inhibition by C-III was not reversed to any significant extent by either increased concentration of activator or triglyceride in the substrate. Our previous studies have shown that in a type III hyperlipoproteinemia (broad-beta-disease) a post-heparin plasma lipoprotein lipase activated by C-II polypeptide of lipoprotein C is decreased in enzyme activity and exhibits an impaired ability to hydrolyze triglycerides in very low density lipoproteins. Type III patients are characterized by elevated concentrations of ApoE in the serum. The data presented in this report suggest that the decreased C-II activated lipoprotein lipase may be further aggravated by increased ApoE levels. Since this enzyme is involved in the catabolism and removal of lipoproteins, decreased activity of C-II activativated lipoprotein lipase may presumably be responsible for increased ApoE.
Keywords:Reprint requests should be addressed to Devaki Ganesan   M.D.   Cardiovascular Research Program   Oklahoma Medical Research Foundation 825 N.E. 13th Street   Oklahoma City   Okla. 73104.
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