Effect of chlorophenoxyisobutyrate on rat liver non-saponifiables

1968 ◽  
Vol 46 (1) ◽  
pp. 81-84 ◽  
Author(s):  
W. E. J. Phillips ◽  
M. R. Lakshmanan ◽  
R. L. Brien
Keyword(s):  
Enzyme Activity ◽  
Vitamin A ◽  
Rat Liver ◽  
Serum Cholesterol ◽  
Reductase Activity ◽  
Liver Weight ◽  
Liver Cholesterol ◽  
Total Liver ◽  
Cholesterol Levels

Chlorophenoxyisobutyrate (CPIB) when fed in the diet at 0.2% for periods of from 3 to 25 days increased liver weight by 28% and increased total liver ubiquinones by 75%. This increase did not change succinate-neotetrazolium reductase activity. Although serum cholesterol levels were significantly reduced, no changes were observed in total liver cholesterol or vitamin A. The data suggest that this hypocholesterolemic agent, although it increases ubiquinone, does not adversely affect the above enzyme activity nor does it modify vitamin A utilization as determined from liver stores.

Suppression of hepatic cholesterogenesis in the rat by lithium ion

1968 ◽  
Vol 46 (2) ◽  
pp. 135-139 ◽  
Author(s):  
R. S. Leal ◽  
M. L. M. Lyra
Keyword(s):  
Rat Liver ◽  
Serum Cholesterol ◽  
Biosynthetic Pathway ◽  
Lithium Ion ◽  
Mevalonic Acid ◽  
Liver Cholesterol ◽  
Cholesterol Levels ◽  
Cholesterol Biosynthetic Pathway ◽  
Ion Incorporation ◽  
Hepatic Cholesterogenesis

The effects of lithium ion on the rates of incorporation of acetate-1-14C and mevalonic-2-14C acid into cholesterol, on 14CO2 production and acetoacetate formation from carboxyl-labeled acetate, on serum and liver cholesterol levels, and on the acetate-activating system were studied in rat liver.It has been found that while the incorporation of labeled acetate into cholesterol was strongly suppressed by lithium ion, incorporation of mevalonate into cholesterol under the same conditions was virtually unchanged. It thus appears that lithium ion produces its effect prior to the formation of mevalonic acid in the pathway of cholesterol biosynthesis.Liver cholesterol levels are practically unchanged after 4 weeks' treatment with lithium chloride while serum cholesterol, under the same conditions, appears to be slightly increased in the treated animals. 14CO2 production and acetoacetate formation from carboxyl-labeled acetate, and the acetate-activating system of rat liver appear to be slightly impaired by lithium ion. The possibility of the existence of more than one block between acetate and mevalonic acid on the cholesterol biosynthetic pathway is discussed.

Glycerol as an inhibitor of cholesterol synthesis

1968 ◽  
Vol 46 (8) ◽  
pp. 859-863 ◽  
Author(s):  
B. B. Migicovsky
Keyword(s):  
Total Cholesterol ◽  
Rat Liver ◽  
Serum Cholesterol ◽  
Cholesterol Synthesis ◽  
Specific Radioactivity ◽  
Cholesterol Concentration ◽  
Liver Cholesterol ◽  
Water Control ◽  
Glycerol Water ◽  
Serum Cholesterol Concentration

The supernatant from a homogenate of rat liver was incubated in a system containing 14C-acetate. The mixture was then saponified, the cholesterol isolated as the digitonide, and its radioactivity determined. When glycerol (water control) was a constituent of the incubation mixture, less radioactivity appeared in the digitonide. Under the same conditions, glycerol did not apparently inhibit the incorporation of 14C-mevalonate into liver cholesterol. When rats were given glycerol or glucose by mouth then 14C-acetate intraperitoneally, the total cholesterol radioactivity, specific radioactivity, and in most cases the serum cholesterol concentration, were all lower in those rats that had been given the glycerol.

VARIOUS EFFECTS OF THYROXINE ANALOGUES ON THE HEART AND SERUM CHOLESTEROL IN THE RAT

1960 ◽  
Vol 21 (1) ◽  
pp. 25-32 ◽  
Author(s):  
G. S. BOYD ◽  
M. F. OLIVER
Keyword(s):  
Heart Rate ◽  
Oxygen Consumption ◽  
Serum Cholesterol ◽  
Rate Ratio ◽  
Heart Weight ◽  
Liver Cholesterol ◽  
Response Curves ◽  
Experimental Conditions ◽  
Cholesterol Levels ◽  
Stimulation Of

SUMMARY A series of twelve iodinated thyroxine analogues was studied for thyro-activity in the rat. Each analogue produced antigoitrogenic activity, increased oxygen consumption, heart rate and heart weight, and decreased serum and liver cholesterol levels. A 'serum cholesterol/heart rate ratio' may be computed for these analogues under fixed experimental conditions. While the dose-response curves for different analogues in any of these assays are rarely parallel, it is, nevertheless, clear that under certain experimental conditions some iodothyronines cause a relatively greater depression of cholesterol levels and less stimulation of heart rate than others. Some of the most active in this respect are DT4, DT3, DT2 and T4F.

DIETARY MARINE FISH OILS AND CHOLESTEROL METABOLISM: 2. THE EFFECT OF VITAMIN A AND LINGCOD LIVER OIL COMPONENTS ON THE SERUM CHOLESTEROL LEVELS IN CHICKS

1960 ◽  
Vol 38 (8) ◽  
pp. 879-887 ◽  
Author(s):  
J. D. Wood
Keyword(s):  
Vitamin A ◽  
Aluminum Oxide ◽  
Dietary Supplement ◽  
Serum Cholesterol ◽  
Cholesterol Metabolism ◽  
Fish Oils ◽  
Cholesterol Feeding ◽  
Cholesterol Levels ◽  
Oil Components ◽  
Aluminum Oxide Column

Lingcod liver oil unsaponifiable material was separated into three main fractions by means of an aluminum oxide column. Major components of the three fractions were vitamin A, cholesterol, and glyceryl ethers, respectively. These fractions were given as dietary supplements to cholesterol-fed chicks and the effect of the supplements on the hypercholesterolemia induced by the cholesterol feeding was investigated. The fraction containing vitamin A prevented the hypercholesterolemia. Crystalline vitamin A acetate produced a similar effect when it was added as a dietary supplement. It was concluded that vitamin A was probably the hypocholesterolemic agent in lingcod liver oil although other compounds in the oil may also exert some influence on the control of the serum cholesterol concentrations in the chicks.

ON THE MODULATING EFFECTS OF OVARIES ON NEONATAL ANDROGEN PROGRAMMING OF RAT LIVER ENZYMES

1975 ◽  
Vol 78 (2) ◽  
pp. 294-301 ◽  
Author(s):  
Åke Stenberg
Keyword(s):  
Enzyme Activity ◽  
Rat Liver ◽  
Liver Enzymes ◽  
Testosterone Propionate ◽  
Reductase Activity ◽  
Female Rats ◽  
Time Of Death ◽  
Hepatic Enzyme ◽  
Enzyme Activity Pattern ◽  
Reversible Nature

ABSTRACT The metabolism of 4-[4-14C]androstene-3,17-dione in rat liver microsomal and cytosol fractions was investigated in adult female rats treated with 1.45 μmole of testosterone propionate at birth. The effects of ovariectomy at 14 and 43 days of age on neonatal testosterone imprinting of enzyme levels were studied. Animals spayed 14 days after birth showed a typical masculinized hepatic enzyme activity pattern with a decreased level of the 5α-reductase activity and increased levels of 5α-reductase, 16α-hydroxylase and 17α- and 3β-hydroxysteroid reductase levels. The pattern was essentially the same in testosterone propionate-treated rats spayed 43 days after birth – with the exception of a feminized 5α-reductase activity – whereas a completely feminized ("de-imprinted") pattern of enzyme activities was found in the rats with intact ovaries at the time of death. It is concluded that de-imprinting action of ovaries is mainly of a reversible nature.

Serum cholesterol levels of inbred rats

1964 ◽  
Vol 207 (3) ◽  
pp. 631-633 ◽  
Author(s):  
David Kritchevsky ◽  
Shirley A. Tepper
Keyword(s):  
Body Weight ◽  
Serum Cholesterol ◽  
Inbred Strains ◽  
Female Rats ◽  
Male Rats ◽  
Liver Cholesterol ◽  
Cholesterol Levels ◽  
Male And Female Rats ◽  
Males And Females ◽  
The Mean

Changes in serum cholesterol levels with age have been studied in male and female rats of three inbred strains (BN, DA, and Lewis) and one random-bred strain (Wistar). The mean serum cholesterol levels at each age differed among strains. Serum cholesterol levels (mg/100 ml) for male rats at 30, 60, and 90 days were: BN-65, 46, and 47; DA-105, 85, and 101; Lewis-79, 76, and 57; and Wistar-64, 63, and 73. For female rats the values were: BN-56, 45, and 47; DA-86, 74, and 91; Lewis-77, 83, and 67; and Wistar-59, 71, and 83. The variation of serum cholesterol with age was different between strains, but similar for males and females within each strain. There was no correlation between body weight and serum cholesterol. Liver cholesterol levels (mg/100 g) determined at 90 days were, for the males, BN-187, DA-233, Lewis-247, and Wistar-300, and for the females, BN-188, DA-244, Lewis-216, and Wistar-249. No correlation with body weight or serum cholesterol was observed.

Cholesterol-mediated regulation of HMG-CoA reductase in microsomes from human skin fibroblasts and rat liver

1990 ◽  
Vol 68 (3) ◽  
pp. 674-679 ◽  
Author(s):  
R. George ◽  
P. J. Davis ◽  
L. Luong ◽  
M. J. Poznansky
Keyword(s):  
Tissue Culture ◽  
Enzyme Activity ◽  
Human Skin ◽  
Rat Liver ◽  
Reductase Activity ◽  
Cholesterol Content ◽  
Skin Fibroblasts ◽  
Human Skin Fibroblasts ◽  
Hmg Coa Reductase ◽  
Coa Reductase

3-Hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase activity was determined in microsomes from human skin fibroblasts and rat liver that had been variously manipulated in vivo or in tissue culture to up- and down-regulate the enzyme. The cholesterol content of these microsomal preparations was then altered by depletion to or enrichment from either cholesterol-free or cholesterol-rich lipid vesicles. Microsomes from human skin fibroblasts responded to cholesterol depletion by increasing HMG-CoA reductase activity and by decreasing it in response to cholesterol enrichment. This was independent of the initial enzyme activity or the tissue culture conditions. Alterations in cholesterol content of rat liver microsomes in vitro failed to demonstrate any significant changes in HMG-CoA reductase activity whether the microsomes started with low enzyme activity (cholesterol-fed rats) or with high enzyme activity (cholestyramine-treated rats). The results are discussed in relation to previously published data and in respect to differences in the control of the human skin fibroblast and rat liver enzymes.Key words: cholesterol, HMG-CoA reductase, microsomes, fibroblasts, rat liver.

Sign in / Sign up

Export Citation Format

Share Document