The metabolism of transferrin was studied using purified '*'I-labeled transferrin in 11 alcoholic patients; six with fatty liver and five with cirrhosis. Six healthy subjects whose alcohol intake was les than 40 gm daily were studied as a control group.
There were no significant differences in the mean fractional catabolic rate and plasma volume in the alcoholic groups when compared with control subjects. A significantly decreased mean serum transferrin concentration was found in the alcoholic cirrhotic patients (1.8 f 0.3 gm per liter vs.
2.9 f 0.2; p < 0.01), resulting from diminished total body synthesis (0.9 f 0.2 mg per kg per h r vs. 1.8 f 0.2; p c 0.01). In contrast, in the patients with alcoholic fatty liver, the mean total body transferrin synthesis (2.4 f 0.3 mg per kg per hr) was significantly increased when compared with controls (p < 0.05).
For all the alcoholic patients, the serum transferrin correlated with transferrin synthesis (r = +0.70; p < 0.01) but the serum iron did not.
These results suggest that, in alcoholic cirrhosis, transferrin synthesis is decreased, probably reflecting diminished synthetic capacity by the liver. In contrast, in patients with alcoholic fatty liver, transferrin turnover is accelerated.
Alcoholic liver disease is often associated with disorders of iron metabolism. These include alterations in plasma iron turnover (l), red cell iron incorporation (1, 2) depression of serum transferrin concentration (3) and, in approximately one-third of chronic alcoholics, an increase in liver iron concentration (4). In the rat, ethanol has been shown to alter the rate of exportable protein synthesis by the liver, particularly transferrin, which is the major serum iron transport protein (5-7).
As transferrin is synthesized by the liver, liver damage may, per se, alter the rate of transferrin synthesis. Although the lowered serum transferrin concentrations seen in many alcoholic cirrhotics may simply reflect depressed protein synthesis, it is possible that alcohol may exert an additional effect on transferrin metabolism.