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Biomedical subjects

S A Tepper

Publications and source records attributed to S A Tepper.

At least 55 records · Page 3Linked to original sources
PubMed1978

Cholesterol vehicle in experimental atherosclerosis. Part 16. Effect of peanut oil on pre-established lesions.

Rabbits were fed an atherogenic diet (2% cholesterol and 6% corn oil) for 8 weeks and then divided into groups of equal average serum cholesterol levels. One group was autopsied, and the others were returned to cholesterol-free diets consisting of commercial laboratory ration or ration augmented with 6% corn oil, peanut oil or PGF, a fat designed to resemble peanut oil minus arachidic and behenic acids. The animals were maintained on the diets for 8 more weeks. On all regimens, severity of atherosclerosis was exacerbated. The extent of exacerbation was significantly less in rabbits fed corn oil than in the others. The extent of exacerbation of lesions appears to be a function of the level of unsaturation of the dietary fats.

Animals↗
PubMed1977

Linoleic acid amides: effect on cholesteremia and atherosclerosis.

Several of a series of linoleic acid amides have been reported to inhibit cholesterol-induced atherosclerosis in rabbits. The three amides which have been studied to the greatest extent are (in order of increasing activity) N-cyclohexyl linoleamide (AC23), N(alpha methylbenzyl) linoleamide (AC223), and N[aplha-phenyl-beta-(p-tolyl)ethyl] linoeamide (AC 485). We have found AC223 to inhibit cholesterol absorption in rats and to slightly inhibit exogenous but not endogenous cholesteremia in rabbits. In a fiber-free diet, AC223 reduces serum cholesterol and liver triglyceride levels. Rats were also fed a basal semipurified diet with and without AC223. Fecal excretion of labeled exogenous (as [ (14)C] cholesterol) or endogenous (as [14 C] mevalonolactone) steroid was 44 and 43% higher in drug treated groups. The mechanism of hypocholesteremic action of the linoleamides appears to involve inhibition of cholesterol absorption.

Amides↗
PubMed1977

Cholesterol vehicle in experimental atherosclerosis. Part 15. Randomized butter and randomized lard.

Randomized lard and butter oil were conpared with native lard and butter oil for their effects on cholesterol-induced atherosclerosis in rabbits. In each experiment there was also a group fed corn oil. The diets contained 2% cholesterol and 6% fat and were fed for eight weeks. Randomization of either butter or lard had virtually no effect as regards their atherogenic potential when fed as part of a diet containing 2% cholesterol. The corn oil-containing diet was less atherogenic than any of the other fats.

Animals↗
PubMed1977

Experimental atherosclerosis in rabbits fed cholesterol-free diets. Part 7. Interaction of animal or vegetable protein with fiber.

Rabbits were maintained for 10 months on a semipurified, cholesterol-free atherogenic regimen. All diets contained sucrose (40%) and hydrogenated coconut oil (14%). The protein (25%) was either casein or soya protein and the fiber (15%) was either wheat straw, alfalfa, or cellulose. Within either protein group the order for induction of cholesteremia was cellulose=wheat straw greater than alfalfa. For atherogenesis, the effect was cellulose greater than wheat straw greater than alfalfa Soya-wheat straw or soya-cellulose diets were less cholesteremic and atherogenic than their casein counterparts. When alfalfa was the fiber, the two types of protein were almost equivalent. Our results show that casein may be more cholesteremic and atherogenic than soya protein under certain conditions (cellulose or wheat straw as fiber) but the addition of alfalfa to the diet renders the two proteins equivalent.

Animals↗
PubMed1976

Age-related changes in the lipid metabolism of Fisher 344 rats.

Lipid metabolism of male Fisher 344 rats aged 2-24 months was studied. Serum and liver cholesterol levels did not display the age-related gradual increase seen in other rat strains. An increase in the serum plus liver cholesterol pool from 2 to 6 months was followed by a plateau through 18 months and then another increase at 24 months of age. The triglyceride pool increased from 2 to 6 months and then remained unchanged through 24 months of age. Cholesterol synthesis from acetate decreased 50% between 2 and 9 months and fell only slightly through 24 months of age. Assay of 3-hydroxy-3-methyl glutaryl Coenzyme A (HMG-CoA) reductase showed a similar pattern but did not decrease further after 9 months of age. Cholesterol 7alpha hydroxylase activity was not significantly altered by age. These age- and strain-related differences present an opportunity for a comparative study of the aging process using the parameters of lipid metabolism as indicators.

Acetates↗
PubMed1976

Influence of ketamine, phenylcyclidine, and phenobarbital on cholesterol metabolism in rats.

The effects of ip injections of phenobarbital (100 mg/kg), phenylcyclidine (Sernylan; [1-(1-phenylcyclohexyl)-piperidine-HBl] (1 mg/kg), and ketamine (Ketaset; [dl)2-O-chlorophenyl)-2-(methylamino)cyclohexanone-HCl] (1 mg/kg) on lipid metabolism in rats were compared. This study was undertaken to determine whether the two sedatives currently used in primates share any of the undesirable effects of phenobarbital on lipid metabolism. All three compounds were administered to male Wistar rats for 6 days. Phenobarbital was hepatomegalic, stimulated 7alpha hydroxylation of cholesterol, and inhibited cholesterol synthesis by rat liver slices from mevalonate, but not acetate. The two other sedatives exhibited effects very similar to those observed in the controls. From our work in rats it is concluded that the use of Sernylan or Ketaset for sedation of nonhuman primates will not significantly affect these parameters of lipid metabolism.

Animals↗
PubMed1976

Influence of four agents (tibric acid, DH 990, oxandrolone and Sch 9122) on aspects of lipid metabolism in rats).

We have investigated the effects of four drugs on aspects of lipid metabolism in rats. The four drugs used were: tibric acid = 2-chloro-5-(cis--3,5-dimethylpiperidonosulfonyl)benzoic acid; DH 990 = 2-[(3,5-di-t-butyl-4-hy-droxyphenyl)thio]hexanoic acid; oxandrolone = 17beta-hydroxyphenyl-17a-methyl-2-oxa-5a-androstan-3-one; and Sch 9122=2-(p-anisyl)-3(2-pyridyl)pentane hydrochloride. Serum and liver triglycerides and liver cholesterol, 7a-hydroxylase and 26-oxidase were determined. Tibric acid (0.015%) was hepatomegalic and hypotriglyceridemic. It did not affect normal 7a-hydroxylase or 26-oxidase activity. In the absence of cytosal, this drug resulted in normal mitochondrial cholesterol-26-oxidase activity whereas none was observed with preparations from control rats. DH 990 (0.075%) did not affect liver size. It had a slight (10--20%) hypolipidemic effect. The effects of DH 990 on the two liver enzymes were similar to those of tibric acid. In view of the absence of a hepatomegalic effect of DH 990, its influence on mitochondrial oxidation of cholesterol in the absence of cytosol is noteworthy. Oxandrolone (0.15%) had a slight (11%) hepatomegalic effect but did not influence serum of liver lipid levels. This drug caused a 19% increase in liver 7a-hydroxylase activity but did not affect cholesterol-26-oxidase activity in the presence or absence of cytosol. Sch 9122 (0.03%) caused significant weight loss. Serum and liver cholesterol levels were unaffected, but serum triglyceride levels were significantly elevated in rats fed this drug. Cholesterol-7a-hydroxylase activity was slightly (11%) higher than normal, but 26-oxidase was significantly lower.

Animals↗
PubMed1975

Influence of an eggplant (Solanum melongena) preparation on cholesterol metabolism in rats).

To investigate the mechanism behind the hypocholesteremic properties of Solanum melongena diets containing 1% Sol. mel. leaf or fruit powder, alfalfa, or clofibrate were fed to rats. Sol. mel. did n ot lower the serum plus liver cholesterol pool of rats, whereas alfalfa and clofibrate did. However, all substances tested decreased the absorption of a single dietary dose of [4-14C] cholesterol. It appears that Sol. mel. exerts its reported hypocholesteremic effect in rabbits through an inhibition of absorption of dietary cholesterol. This inhibition is probably brought about partially through the binding of bile salts which are essential for cholesterol absorption.

Animals↗