A rat model was used to investigate the effects of starvation and protein depletion on serum fibronectin levels and reticuloendothelial function. Serum fibronectin levels decreased significantly following both test diets. The uptake of opsonin-independent test agents was minimally affected by starvation and protein depletion. Clearance of gelatinized colloidal carbon, which is dependent on circulating opsonins, was significantly reduced in the malnourished animals. This clearance defect was corrected by incubation of colloidal carbon with normal serum. These data suggest that reticuloendothelial dysfunction secondary to malnutrition is primarily mediated by a deficiency of circulating opsonins.
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