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Biomedical subjects

J W Erdman

Publications and source records attributed to J W Erdman.

98 records · Page 6Linked to original sources
PubMed1981

Hyperlipidemia in rats fed retinoic acid.

This report describes a series of experiments that attempt to characterize the lipidemia accompanying retinoic acid administration. After feeding young adult male Sprague-Dawley rats, 1.2 Retinol Equivalents (R.E.) retinyl acetate plus supplemental retinoic acid (100 microgram/g dry diet) for three days and fasting for 6-8 hr, triglyceride, cholesterol, and phospholipid content of various serum lipoprotein fractions were determined. When compared to unsupplemented controls, both the serum very low density lipoprotein (VLDL) and the high density lipoprotein (HDL) fractions of the retinoic acid-fed rats were found to harbor an elevated triglyceride content. While VLDL cholesterol and phospholipid content were also elevated, total serum cholesterol and phospholipids were not statistically altered. The detergent Triton WR-1339 was used to depress serum triglyceride clearance in order to assess the effects of retinoic acid feeding on serum triglyceride levels. Triglyceride accumulation started earlier after Triton treatment and was greater when rats were fed 100 microgram/g retinoic acid for three days prior to testing. Red and white gastrocnemius muscle, cardiac ventricular muscle, and perirenal adipose tissue were removed from rats following retinoic acid feeding. Analysis of these tissues for lipoprotein lipase (EC 3.1.1.3) activity showed a decrease in adipose tissue, a large depression in both areas of gastrocnemius muscle and no change in cardiac muscle as a result of retinoic acid feeding.

Animals↗
PubMed1980

Vitamin A induced hypertriglyceridemia in cholesterol-fed rats.

The effects of level and feeding frequency of retinoic acid (OIC) or retinyl acetate (YL) on the accumulation of lipids in the serum and liver of rats were investigated. Male Sprague-Dawley rats were fed ad libitum 1% cholesterol diets with or without supplemental OIC or YL. Vitamin A-fed groups included (per g of dry diet): 105 microgram of OIC or 113 microgram YL daily for 28 days, 735 microgram OIC or 791 microgram YL once each week for 28 days; and 735 or 105 microgram OIC on day 1 or 105 microgram OIC daily for the week experiment. Daily feeding of OIC or YL increased serum triglyceride concentrations as compared to conrols. Several days after removal of OIC or 1 week after removal of supplemental YL from the rat diets, serum triglyceride concentrations returned to basal levels. Cholesterol feeding elevated serum cholesterol as well as hepatic cholesterol, total lipids and vitamin A concentrations. Daily OIC feeding depressed serum and hepatic cholesterol concentrations. These results show that daily supplement of vitamin A increased serum triglycerides and reduced serum and hepatic cholesterol concentrations. Serum and liver alterations were dependent on continued feeding.

Animals↗
PubMed1980

Comparative effects of all-trans and 13-cis retinoic acid administration on serum and liver lipids in rats.

The effects of all-trans and 13-cis retinoic acid upon serum and liver lipids were investigated in Sprague-Dawley rats. Groups of rats were fed daily with 105, 210 and 315 micrograms/g diet of one of the retinoids for periods of up to 8 days. Other groups were injected intraperitoneally (I.P.) daily with retinoids at levels equivalent to the daily intake of rats receiving 105 or 210 micrograms of retinoid/g diet. All dietary concentrations of all-trans retinoic acid induced hypertriglyceridemia, however, only the highest dietary concentration of the 13-cis form caused this response. Injection of the all-trans form consistently increased serum triglycerides, while 13-cis retinoic acid did so in only one case. Retinoid-fed rats fasted for 6 hours before blood sampling demonstrated similar increases in serum triglycerides compared to their respective controls. Also, retinoid administration reduced serum retinol at all levels tested with the all-trans form appearing to be more potent. Growth and feed intake was somewhat reduced in rats receiving the highest level of all-trans retinoic acid. Liver analysis did not reveal fatty liver or alterations in phospholipid, cholesterol, or vitamin A content in any groups monitored. Our previous studies have shown induction of hypertriglyceridemia when rats were fed as low as 26 micrograms/g diet of all-trans retinoic acid. The current studies would indicate that feeding 315 micrograms/g diet of the 13-cis isomer was required to elicit a similar response.

Animals↗
PubMed1979

Effect of retinoic acid and retinyl acetate feeding upon lipid metabolism in adrenalectomized rats.

Many reports have appeared in the literature suggesting that vitamin A may exert some of its effects via changes in adrenocortical activity. A series of experiments were performed in order to assess the possible role of the adrenal gland in vitamin A-induced lipid alterations in rats. Adrenalectomized, sham-operated, and intact rats were fed retinoic acid or retinyl acetate at several levels. Either 25 or 100 retinol equivalents (RE)/g dry diet were fed to male Sprague-Dawley rats for periods of 7 or 28 days. Neither compound had an effect on the concentration of liver glycerides, phospholipids, cholesterol, or total lipids. Vitamin A, especially in the form of retinoic acid, was found to induce an elevation of plasma triglycerides. The presence of the adrenal gland was not necessary for the induction of hypertriglyceridemia nor was there any indication of increased adrenocortical output (as measured by plasma corticosterone level) as a result of vitamin A feeding. There was a reduction in circulating retinol as a result of retinoic acid feeding at either 25 or 100 RE in sham-operated and adrenalectomized rats but not in unoperated rats. These experiments demonstrate that vitamin A, especially in the form of retinoic acid, fed at as low as 25 RE/g diet to the rat can induce hypertriglyceridemia, and that the adrenal gland does not mediate this effect.

Adrenal Glands↗