Fatty Infiltration in the Liver—Response to Treatment

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INFILTRATION of fat in the liver may be produced experimentally in animals by dietary restriction of proteins, choline and precursors of choline, vitamin-B complex, as well as by the administration of hepatotoxins. Von Mering and Minkowski,1 in studying diabetes, reported in 1890 the frequent occurrence of fatty liver in depancreatized dogs. In 1924, Allan, Bowie, Macleod, and Robinson,2 and Fisher3 noted that large fatty livers developed in depancreatized dogs maintained on insulin for long periods. These findings led one of us (C.H.B.4) to suggest that liver function studies should be conducted on all diabetic patients.

In 1932, Best, Hershey, and Huntsman5 by dietary means produced fatty infiltration in the livers of normal rats in about three weeks, while six months was required for similar changes to appear in the depancreatized dog. Chaikoff and associates6, 7 produced definite cirrhotic changes both in pancreatectomized and in normal dogs by prolonged feedings of diets that stimulated the accumulation of fat in the liver. Subsequently, several other investigators reported similar lesions occurring in rats on deficient diets.

Best, Hartroft, and Sellers8 reported that in experimental animals on a low-choline diet, stainable lipids first appeared in the liver as small intracellular globules. Subsequently the globules coalesced to form large spherical masses distending the cell membrane. The membranes of the liver cells, distended with fat, were increasingly stretched until the cell membranes broke and fatty cysts were formed in from six to nine weeks. With the rupture of the fatty cysts, definite cirrhotic changes occurred with . . .



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