| First Author | Williams S | Year | 1986 |
| Journal | Mouse News Lett | Volume | 74 |
| Pages | 115 | Mgi Jnum | J:14087 |
| Mgi Id | MGI:62264 | Citation | Williams S, et al. (1986) High cholesterol diet leads to increased levels of liver apolipoprotein A-IV mRNA. Mouse News Lett 74:115 |
| abstractText | Full text of MNL contribution: High cholesterol diet leads to increased levels of liver apolipoprotein A-IV mRNA. Apolipoprotein A-IV (Apo A-IV) is a protein involved in cholesterol and lipid transport and absorption. It is normally synthesized in a tissue-specific manner in mouse liver and small intestine, as determined by quantitation a t both the protein and mRNA levels. We have previously shown that the level of liver Apo A-IV mRNA increases in response to porphyria (diseases caused by disruptions in porphyrin-heme biosynthesis, Buchberg and Kinniburgh (1985) NAR 13: 1953-1963). We wish to define a more direct relationship between induction of Apo A-IV and dietary cholesterol. We have, therefore, prepared liver RNA from 64 mice, including parental inbred and recombinant inbred mouse lines, that had been fed a high cholesterol diet for 15 weeks. These RNAs were analyzed by Northern blotting using a mouse cDNA probe of Apo A-IV. We find that: 1) the C57BL/6J gene produces a low basal level of Apo A-IV mRNA and is highly inducible by increased cholesterol; and 2) the C3H/HeJ and BALB/cJ genes produce a higher basal level of Apo A-IV mRNA but are unaffected by increased cholesterol. These results indicate that there may be two alleles of the Apo A-IV gene in the mouse population. The recombinant inbred lines tested support this hypothesis, carrying either one of the parental alleles. The connection between the induction of Apo A-IV mRNA seen in porphyria and that seen in response to elevated cholesterol levels is not clear at this point, but we intend to examine their relationship by feeding porphyric mice on elevated cholesterol diets and looking at the effect on Apo A-IV mRNA levels. (S. Williams, S. Hunter (Trinity College, Dublin), A. Lusis (UCLA, Medical Center, Los Angeles) and A. Kinniburgh) |
