C. C. Lucas

THE LIPOTROPIC FACTORS

The nutritional role of choline was in 1932, so that this year it comes of age as a dietary factor. Choline was the first of the accessory food factors which was shown to protect the liver; i.e., in its absence from the diet, pathological changes appear promptly in the hepatic cells. The work on choline, as a survey of the literature clearly shows, stimulated great interest in liver fat, in the effect of large accumulations of fat on hepatic function, and in the part played by other dietary factors in the protection of the liver. The very general and broad title assigned to us here has made us somewhat uncertain about what is desired. The topics to be dealt with by our learned colleagues on this comprehensive program leave us but little in the way of definite responsibility, and we are therefore quite free to discuss certain general aspects of our subject. We are all familiar with the fact that choline, betaine, methionine and, under some conditions, vitamin B I ~ and inositol, protect rats in varying degrees against the development of fatty livers. I n the absence of choline from the diet, many species of animals have been found to develop this abnormality. The rat,l* *, 5 mouse,3’ rabbit,8 h a m ~ t e r , ~ calf,I0 pig,” and ducklingI2 exhibit fatty livers when the diet lacks sufficient of the lipotropic agents, choline or its precursors. Some of the classical lesions are illustrated in Professor Hartroft’s presentation (page 633). I n some species, such as the guinea pig, it is very difficult to produce an abnormal deposition of fat in the liver by feeding diets low in ch01ine.’~ We must always keep in mind that interference with the function of hepatic cells by means other than deficiency of the lipotropes may lead to fatty livers. Fatty livers of guinea pigs on scorbutic diets14 are probably not attributable to a lack of dietary choline. Many readers are doubtless familiar with the hemorrhagic kidney syndrome15 which may be consistently produced in young rats on diets low in the lipotropes. With the hypolipotropic diets currently used in our laboratory we are able consistently to produce kidney lesions in mature animals. Somewhat similar renal lesions have been reported in young p i g P and calves.1° The failure to produce this kidney lesion in young mice and puppies, both of which develop fatty livers readily enough, reveals a problem which may possibly require extended study. A comprehensive investigation and comparison of the relevant enzyme systems will undoubtedly help. An interesting sequel to the renal lesion in rats is the appearance in later life of hypertension.” This has not yet been reported in other species. You are also familiar with the failure of baby chicks,’* turkey poults19 and ducklings“o* to grow and their tendency to develop slipped tendon disease on choline-deficient diets. In our early studies on the effects of choline in preventing and curing the pathological changes in the diabetic dog, we mentioned “areas of beginning fibrosis” which did not appear to be as favorably affected by choline as the fatty changes,22

Solubility of tissue phosphatides in acetone

Abstract Treatment of plant and animal tissues with acetone extracted considerable amounts (from about 10 to 95%) of the total phosphatides. Of the animal organs tested, muscle gave up the largest proportion of its phosphatides to acetone, brain the least. Considerable unsuspected loss of phosphatides may occur if acetone is used for preliminary drying of tissues or to remove simple lipides.