The mechanism of CCl4-induced fatty liver was investigated, studying biochemical changes and phospholipid metabolism in mitochondria and microsomes of CCl4-poisoned rat liver. Rats were sacrificed 2, 4, 8, 12 and 24 hours after the intraperitoneal administration of CCl4. The mitochondrial respiratory control was intact during the first 8 hours of intoxication, but disturbed in 12 hours. The mitochondrial oxidative phosphorylation was disturbed 24 hours after the injection of CCl4. Changes in the fatty acid composition of mitochondrial phospholipids occurrd 12 hours after CCl4-injection when the mitochondrial respiratory control began to be disturbed. These changes became remarkable thereafter: arachidonic acid decreased, palmitic, stearic and oleic acid increased. On the other hand the fatty acid composition of microsomal phospholipids changed in earlier stage, already 2 hours after CCl4-injection and became remarkable during the course of poisoning: arachidonic acid decreased, palmitic, oleic and linoleic acid increased. The changes of the fatty acid composition of microsomal phospholipids were coincident with the decrease of cytochrome b5 and P-450. The changes of fatty acid patterns in the phospholipids correspond with the increase of neutral fat in the fatty liver and have intimate relation with the functional depression due to the destruction of integrity of the subcellular particles. From above data it is suggested that CCl4-administraction causesthe destruction of the integrity of subcellular particles in situ and that, therefore, microsomal changes are the primary cause of the fatty liver induced by CCl4.
After inducing the proliferation of bile ductules in the liverof rats by feeding them on a DAB diet, broken rice with DAB at the rate of 0.06 percent, butreverting to pulverized rice before cancer development, cytological changes in the course ofregeneration were compared with those changes in the proliferation processes for thepurpose to determine whether or not proliferated bile ductules would differentiate into liver cells and also to study changes in bile ductules elicited by a partial hepatectomy. This communication deals briefly with the results of the study. 1)Bile ductules showed a distinct cytological difference between the proliferation and regeneration stage. Namely, it was possible to differentiate these bile ductules into three types; one with oval nucleus and moderately abundant cytoplasm that appeared to be budding off from the bile duct, the other with rather round nucleus undergoing karyokinesis and abundant cytoplasm, and the third with spindle-shaped nucleus and poor cytoplasm. 2)As for the question whether proliferated bileductules can differentiate into liver cells, at least in the regeneration stage although bile ductules undergo morphological changes, they cannot be considered to be definitely being converted to liver cells and even by the observations with reconstruction model it is reasonable to assume that bile ductule is clearly communicated only with the bile duct and it has dead-end on the side of liver cells, hence it does not change into liver cell. 3)It has been clarified that by changing the DAB diet to pulverized rice the bile ductules induced in the rat liver by DAB feeding are reduced in number while liver cells proliferate, and the time required for the disappearance of these bile ductules is over seven times the length of DAB feeding. 4. A partial hepatectomy shows a tendency to enhance the proliferation of bile ductules. 5. When the DAB feeding is changed to broken-rice feeding, the proliferation of bile ductules is inhibited. 6)The intensity of succinic dehydrogenase activity in the liver after a parital hepatectomy is dependent upon the extent of bile ductule proliferation, but it is difficult to ascertain the conversion of bile ductules to liver cells by this fact alone.
Three cases of the postgastrectomized secondary kwashiorkor syndrome were described in the previous reports. In this study, the author made inquiries about 678 gastrectomy patients. They were resected for benign gastric and duodenal disease, and 85% of them answered that their present condition were good. As the result of clinical investigation in 225 cases, there were no cases of severe malnutrition or hypoproteinemia as like as secondary kwashiorkor, but latent malnutritious condition was present because of decreased dietary in take, steatorrhea or decreased body weight. Various absorption tests and pancreozymin-secretin test were done in gastrectomy patients the results in carbohydrate and protein absorption tests differed little from normal subjects, although fat absorption was slightly decreased. The values in pancreozyminsecretin test, volume of duodenal juice, bicarbonate concentration, amylase and lipase and trypsin activities were all higher than those of normal subjects. This was thought that it depended on conpensatoric hyperfunction, but in fact the digestion and absorption were decreased for lack of pancreozymin-secretin stimulation or inadequate mixture of the bile and pancreatic juice to diet. Comparing with gastectomy patients, secondary kwashiorkor patients showed normal absorption of carbohydrate, although reduction of fat and protein absorptions was present, and paticularly protein malabsorption were so servere that this was pointed out to be one of cause in the secondary malnutrition. Pancreozymin-secretin tests corresponded with the above mentioned absorption tests, except amylase test, but bicarbonate concentration, lipase and paticularly trypsin activities were severely decreased. It was thought that this severe malnutrition was resulted from pancreas injury following gastrectomy.
Ulcerative colitis occurring in two brothers, 25 and 16 years ofage, with an interval of approximately 5 years, is decribed. This is the first report in this country in which familial occurrence of ulcerative colitis was noted. The colon of the older brother was totally removed and found to be of typical ulcerative colitis, the changes starting from the rectum and extending to involve the entire colon; the ileum was intact showing a clear boundary between the changed cecal and the normal ileal mucosae. Such distinct confinement of the disease to the colonic mucosa strongly suggests an organ specific disease, and the distinction between the ileal and colonic mucosae. The younger brother exhibited typical but less advanced features of the disease. Steroid therapy has been unsatisfactory in both cases, although some response was noted at the beginning. No etiological relationship has been elicited in these patients, neither was the blood type found to be of significance. It was presumed that constitutional resemblance has provided a basis on which some autoimmune process against colonic mucosa has been initiated. A critical review on familial occurrence of ulcerative colitis has been made.