IntroductionApolipoprotein (apo) E and the two B apolipoproteins, apoB48 and apoB100, are important proteins in human lipoprotein metabolism. Commonly occurring polymorphisms in the genes for apoE and apoB result in amino acid substitutions that produce readily detectable phenotypic differences in these proteins. We studied changes in apoE and apoB phenotypes before and after liver transplantation to gain new insights into apolipoprotein physiology. In all 29 patients that we studied, the postoperative serum apoE phenotype of the recipient, as assessed by isoelectric focusing, converted virtually completely to that of the donor, providing evidence that > 90% of the apoE in the plasma is synthesized by the liver. In contrast, the cerebrospinal fluid apoE phenotype did not change to the donor's phenotype after liver transplantation, indicating that most of the apoE in CSF cannot be derived from the plasma pool and therefore must be synthesized locally. The apoB100 phenotype (assessed with immunoassays using monoclonal antibody MB19, an antibody that detects a two-allele polymorphism in apoB) invariably converted to the phenotype of the donor. In four normolipidemic patients, we determined the MB19 phenotype of both the apoB100 and apoB48 in the "chylomicron fraction" isolated from plasma 3 h after a fat-rich meal. Interestingly, the apoB100 in the chylomicron fraction invariably had the phenotype of the donor, indicating that the vast majority of the large, triglyceride-rich apoB100-containing lipoproteins that appear in the plasma after a fat-rich meal are actually VLDL of hepatic origin. The MB19 phenotype of the apoB48 in the plasma chylomicron fraction did not change after liver transplantation, indicating that almost all of the apoB48 in plasma chylomicrons is derived from the intestine. These results were consistent with our immunocytochemical studies on intestinal biopsy specimens of organ donors; using apoB-specific monoclonal antibodies, we found evidence for apoB48, but not apoB100, in donor intestinal biopsy specimens. (J. Clin. Invest. 1991.

The metabolic disorders known as fatty liver and kidney syndrome and fatty liver-haemorrhagic syndrome are described, and their pathogenesis and aetiology are discussed in relation to current knowledge of the lipid metabolism of the fowl and dietary, environmental and physiological factors which can cause hepatic steatosis.

The occurrence of a 'fishy' or 'crabby' taint in eggs and liver damage culminating in massive haemorrhage has greatly restricted the commercial utilisation of rapeseed meal as a relatively cheap protein supplement for laying hens in the UK. Recent work on these problems is reviewed. It has elucidated the cause of the taint and identified the rapeseed constituents that are involved. A genetic defect impedes the synthesis of trimethylamine oxidase in susceptible hens and goitrin and tannins inhibit the enzyme. This biochemical lesion severely impairs the metabolism of trimethylamine which is released from sinapine and other dietary sources of choline by enteric bacteria. Consequently, excessive amounts pass into the yolk and produce the taint. Liver haemorrhage is associated with hepatocyte degeneration, abnormalities in the biliary system and the leakage of cellular enzymes into the plasma. The toxic substance(s) responsible has (have) not yet been identified.

1. A survey was carried out on dairy farms in the south of Scotland during the period 1958–59 to obtain information on: (a) the mineral element composition of spring pastures associated with grass tetany or staggers and hypomagnesaemia, and (b) the influence of magnesium supplements on the incidence of these conditions and on serum magnesium levels.2. Pastures associated with grass tetany had a significantly lower average magnesium and sodium content and a higher potassium content than those which were classed as normal. These differences were magnified in the values of the ratios K/(Ca + Mg) and (K + Ca + P)/(Mg + Na) which were considerably higher in tetany pastures. The incidence of tetany was positively correlated with the value of the former ratio. These results are similar to those obtained in Holland.3. The analytical results for pastures associated with hypomagnesaemia in clinically normal cows were not significantly different from those for normal pastures and there was no evidence of any association between the composition of the pasture and the incidence or severity of the hypomagnesaemia or the serum magnesium levels.4. The magnesium and sodium contents of the majority of the pastures examined would be judged as inadequate in the light of available information on the requirement of these elements.5. There was no evidence of any correlation between the magnesium content of the pasture and that of any of the other elements studied.6. Cases of grass tetany occurred in 25% of the 108 herds studied, the mean incidence in affected herds being 4·5 ± 0·65%. The overall incidence was 1·1 ± 0·25% and was significantly lower when a magnesium supplement was given as a prophylactic measure.7. Hypomagnesaemia was detected in clinically normal cows after turning out in 41·2% of the herds, the overall incidence being 8·7 ± 1·0%. On tetany free farms the feeding of calcined magnesite or magnesium-rich mineral mixtures did not appear to reduce the incidence of hypomagnesaemia or the fall in serum magnesium levels which occurred after turning out.8. These results emphasize the wide individual variation in the susceptibility of different cows to the factors causing hypomagnesaemia and grass tetany and also the differences between the two conditions in their dietary relationships. It is suggested that dietary factors may be responsible for producing the clinical signs of grass tetany in hypo-magnesaemic cows.