It has previously been shown that, in heavy drinkers, serum apolipoprotein A-I (ApoA-I) levels are closely related to the degree of liver injury: they are at a maximum in patients with steatosis, begin to decrease in patients with fibrosis, and reach a minimum in patients with severe cirrhosis. In contrast with serum ApoA-I variations, serum apolipoprotein B (ApoB) levels are stable. The assessment of messenger RNA (mRNA) levels of ApoA-I and ApoB using a quantitative competitive polymerase chain reaction (PCR) method was performed in 18 alcoholic patients: 8 with normal livers or steatosis (group I), 6 with fibrosis or nonsevere cirrhosis (group II), and 4 with severe cirrhosis (group III). For ApoA-I, group I had higher serum levels (208.4 ± 37.6 mg/dL mean ± SE) and mRNA levels (0.51 ± 0.12) than group II (serum 116 ± 19 mg/dL, P < .01, mRNA 0.40 ± 0.11, P < .09) or group III (serum 56.5 ± 28.6 mg/dL, P < .01, mRNA 0.27 ± .02, P = .008). For ApoB, the three groups had similar serum ApoB levels: 129.9 ± 37.7, 121 ± 51, 120.7 ± 57.4 mg/dL. Group I presented higher levels of ApoB mRNA than those of group III (0.68 ± 0.21 vs. 0.41 ± 0.18, P < .06). There was a significant correlation between serum and mRNA levels of ApoA-I (r = .65, P = .003) but no correlation between serum and mRNA levels of ApoB (r = .19, NS). We suggest that (1) steatosis is associated with increased ApoAI mRNA; (2) fibrosis is associated with decreased serum ApoA-I, probably caused by a posttranscriptional mechanism; (3) severe alcohol-induced cirrhosis is associated with a nonspecific decrease in ApoA-I and ApoB mRNA; and (4) in contrast to ApoA-I mRNA, the ApoB mRNA level makes a slight contribution to the ApoB serum concentration.
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