STUDIES ON THE RAPID ACCUMULATION OF TRIGLYCERIDE IN THE LIVER IN CHOLINE DEFICIENCY

1965 ◽  
Vol 43 (10) ◽  
pp. 1733-1744 ◽  
Author(s):  
Sailen Mookerjea

Studies with isolated liver perfusion preparations showed that, during 5 to 21 days of choline deficiency (acute phase), the livers fail to release any triglyceride into the perfusate, whereas during 1 to 2 days (early phase) and during 28 to 60 days of choline deficiency (prolonged phase), they tend to release triglyceride into the perfusate at a nearly normal rate. The rate of deposition of hepatic triglyceride in intact rats fed a choline-deficient diet showed a progression complementary to this triphasic pattern of triglyceride release, i.e. an early phase of slow triglyceride deposition and an acute phase of rapid accumulation followed by the establishment of a higher steady-state level. In the perfusion experiments changes in phospholipid levels in the perfusate followed the same pattern as the triglyceride levels. Increased uptake of free fatty acids by the choline-deficient livers was most marked after 2 days.In vitro additions of choline and several choline derivatives to the 5-day choline-deficient liver perfusion system were unable to restore triglyceride release. Similar studies with blood obtained from choline-supplemented rats showed a very significant restoration of triglyceride release into the perfusate.

1969 ◽  
Vol 47 (2) ◽  
pp. 125-133 ◽  
Author(s):  
Sailen Mookerjea

Isolated liver perfusion preparations have been used to study the incorporation of glucosamine-1-14C into plasma glycoproteins and glycolipoproteins. The livers obtained from 2-day-choline-deficient rats and perfused with blood obtained from rats on similar dietary treatment showed, compared to controls, an impairment of incorporation of radioactive glucosamine into the trichloroacetic-acid-insoluble protein fraction of plasma during the progress of perfusion. The rate of disappearance of radioactivity in the trichloroacetic-acid-soluble fraction of plasma during perfusion was not affected by choline deficiency. Synthesis of plasma glycolipoproteins as judged by the progressively increased incorporation of radioactivity showed a very significant impairment of synthesis of very low-density (d < 1.006) and low-density (d > 1.006–1.063) glycolipoproteins in early choline deficiency. A similar inhibition of synthesis of plasma proteins of d > 1.21 ("lipid acceptor protein") was observed, whereas the synthesis of high-density lipoproteins (d < 1.063–1.21) was not affected in choline deficiency.The fatty liver in choline deficiency appears to result from an impairment of plasma low-density glycolipoprotein synthesis. A postulation has been made on the stepwise biosynthesis of plasma lipoproteins on the basis of these and earlier studies.


1997 ◽  
Vol 75 (10) ◽  
pp. 1497-1500 ◽  
Author(s):  
PJK Kuppen ◽  
LE Jonges ◽  
CJH van de Velde ◽  
AL Vahrmeijer ◽  
RAME Tollenaar ◽  
...  

1957 ◽  
Vol 35 (1) ◽  
pp. 1-6 ◽  
Author(s):  
R. J. Young ◽  
C. C. Lucas

Young guinea pigs (4–6 days of age) fed a choline-deficient diet grew slowly and died within 3 to 4 weeks, at which time the livers showed only traces of stainable fat. Animals fed the diet supplemented with choline grew at the rate of 5.5 to 6.0 g. per day. Guinea pigs transferred from a complete diet to a choline-deficient diet after 3 to 4 weeks suffered an immediate retardation in growth but no mortality occurred (up to 6 weeks). A decrease in total body fat was noted. After 4 weeks, stainable fat was present in the liver. A small but definite increase in total liver fat occurred at 6 weeks. The guinea pig, like the chick, is unable to place the first methyl group on the ethanolamine moiety of choline, but betaine plus monomethylaminoethanol was as effective as choline in overcoming a deficiency of the latter.


1956 ◽  
Vol 188 (1) ◽  
pp. 45-48 ◽  
Author(s):  
Shirley Weisenfeld ◽  
Raul Hernandez Jauregui ◽  
Martin G. Goldner

Experiments are presented in which insulin solutions were perfused through isolated frog livers in order to study the inactivation of this hormone by liver tissue. The solutions were recirculated many times and aliquots were tested biologically at various intervals for hypoglycemic activity. While insulin retains its activity after a single frog liver perfusion, it is gradually inactivated with increasing numbers of reperfusions. This result is in accord with the inactivation of insulin by liver slices and liver brei as reported by others. The relatively slow inactivation of insulin when perfused through the isolated frog liver is in contrast to the inactivation of glucagon which, as previously reported, loses its hyperglycemic activity after a single perfusion through this preparation. The general significance of this finding is discussed.


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