Phospholipids and component fatty acids of the pigeon liver.

The phospholipids from the livers of adult pigeons were separated by thin layer chromatography and the component fatty acids analyzed by gas liquid chromatography. They consisted of 53.0% phosphatidylcholine, 26.3% phosphatidylethanolamine, 8.6% sphingomyelin, 6.3% cardiolipin and 4.8% lysophosphatidylcholine. Phosphatidylethanolamine and phosphatidylcholine were characterized by a high concentration of long-chain polyunsaturated fatty acids with the highest percentages in the phosphatidylethanolamine. Sphingomyelin contained up to 64.5% saturated acids. About 80% of the fatty acids present in the cardiolipid fraction consisted of linoleic acid. The liver phospholipids had the same composition in lactating as a nonlactating pigeons, but differed in many respects from those available in the crop-milk.

Effect of age and diet on the fatty acid composition of triglycerides and phospholipids from liver, adipose tissue and crop of the pigeon.

The fatty acid pattern of the triglycerides (TG) and phospholipids (PHL) from liver, adipose tissue and crop of the pigeon was studied at various stages of posthatching development to determine the influence of the changing diet. In each tissue and at all ages PHL contained more steric and polyenoic but less monoenoic acids than the corresponding TG. Especially in the young squabs the acid composition of the liver (TG as well as PHL) was different from that of the adipose tissue and the crop. In these last tissues, only small variations were noticed during growth, whereas in the liver the acid pattern changed drastically and specifically for each lipid fraction, mainly in the 1st week after hatching. During the period of only cropmilk feeding (0-4 days) the TG from adipose tissue and crop resembled more the acid pattern of the diet than that of the liver TG, suggesting that in this period these tissues derive their acids for TG synthesis mostly from exogenous sources rather than from the liver. The subsequent change from cropmilk to grain diet was not clearly reflected in the acid content of the examined tissues probably as a result of an enhanced de novo synthesis. The acid distribution in the PHL of the various tissues was at all ages very different from that of the corresponding diets and their alterations, characteristic for each tissue, may therefore be correlated more with age than with dietary conditions.

Development of the lipid and fatty acid patterns of the liver of the pigeon after hatching.

1. The fatty liver of newly-hatched pigeons is caused by an accumulation of sterol esters (STE) amounting to 620 mg/g total lipids of which 80% was sterol oleate. Triglycerides (TG) accounted for only 20 mg/g of total lipids. 2. After hatching, the relative amount of STE in the liver tissue decreased considerably while that of TG increased. The proportion of phospholipids (PHL) remained essentially constant. 3. The fatty acid composition of the liver lipids changed significantly, but specifically for each individual class during postnatal growth. Striking differences were the higher values of long-chain polyunsaturated acids (20: 4 omega 6 and 22: 6 omega 3) in PHL, TG and free fatty acids (FFA) and the higher proportion of oleic acid in the STE at hatching compared with those at older ages. 4. The predominant alterations in the relative composition of the liver lipids (lipid classes and fatty acids) occurred in the first week after hatching and may be accounted for by the decreasing yolk utilisation and adaptation to ingested food. The change within the diet itself from cropmilk to grain (starting around the 4th day) influenced the development of the lipid and fatty acid content only in a minor way. 5. The large weight decreased of the pigeon liver after the 19th day was accompanied by a decrease in absolute PHL content while TG stores were unaltered.

Interactions of native and modified human low density lipoproteins with human skin fibroblasts.

125I-labeled low density lipoprotein (LDL) covalently bonded to Sepharose beads was not degraded by normal human fibroblasts nor did it trigger inhibition of sterol synthesis. The Sepharose beads loaded with LDL bound very tightly to the surface both of normal fibroblasts and fibroblasts from a subject with homozygous familial hypercholesterolemia; control Sepharose beads (activated sites covered with glycine) did not adhere to either cell type. LDL was extracted by a modification of the method of Gustafson (Gustafson, A. (1965) J. Lipid Res. 6, 512-517), so as to remove essentially all cholesterol, cholesterol ester and triglyceride. This modified LDL was bound, internalized and degraded as well as or better than native LDL. However, it failed to suppress sterol synthesis. These results provide additional evidence that the sterol moiety of the LDL is the key component affecting sterol synthesis. They also imply that the neutral lipids of LDL play a minor role in the binding of LDL to cell membranes and that the apoprotein rather than molecular size and shape is the critical factor.