[The hypoglycemic, convulsive and antigenic activity of some purified insulins. Importance of possible differences in the evaluation of the insulin].
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Biomedical subjects
Publications and source records attributed to B Lombardi.
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Previous studies have shown that feeding a choline-devoid (CD) diet to rats is an effective promoter of liver carcinogenesis. In the present studies, we investigated the effects of CD diets containing different levels of fat (high, 15%; low, 4%) on the induction of foci of gamma-glutamyltranspeptidase (GGT) positive hepatocytes in the liver of rats initiated with a single dose of diethylnitrosamine. In rats fed the high-fat CD diet for 4--6 weeks, a greater number of foci was induced than in rats fed similarly the low-fat CD diet. However, liver DNA synthesis and the rate of hepatocyte mitosis were not significantly different in rats fed the 2 CD diets, but were significantly higher than in rats fed a choline-supplemented diet. These results indicate that beside stimulation of liver cell proliferation, other factor(s) determine the efficacy with which a CD diet exerts its promoting action.
Groups of female Fischer-344 rats were fed a semipurified choline-deficient (CD) diet, or a semisynthetic L-amino acid-defined choline-deficient (CDAA) diet, for up to 12 wk and effects of the 2 diets on the liver were compared. Steatosis was diffuse and more severe throughout in rats fed the CDAA diet than in rats fed the CD diet. Greater elevations in serum aspartate and alanine aminotransferase activities were also present in the former rats, along with higher 2-bromodeoxyuridine labeling indices in the liver. Discrete amounts of 8-hydroxyguanine were detected in liver DNA, but were not significantly different in rats fed the 2 diets, or from those present in a group of control rats killed at 0 time. Glutathione S- transferase placental form-positive focal lesions were not observed in any of the rats. The results show that the CDAA diet causes more severe degrees of steatosis and liver cell death and proliferation than the CD diet, raising the possibility that it may, in contrast to the CD diet, result in the eventual induction of hepatocellular carcinomas in female Fischer-344 rats.
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