Essential fatty acid supplemented diet increases renal excretion of prostaglandin E and water in essential fatty acid deficient rats

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Essential fatty acid supplemented diet increases renal excretion of prostaglandin E and water in essential fatty acid deficient rats. / Hansen, Harald S.

In: Lipids, Vol. 16, No. 11, 01.11.1981, p. 849-854.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Hansen, HS 1981, 'Essential fatty acid supplemented diet increases renal excretion of prostaglandin E and water in essential fatty acid deficient rats', Lipids, vol. 16, no. 11, pp. 849-854. https://doi.org/10.1007/BF02535041

APA

Hansen, H. S. (1981). Essential fatty acid supplemented diet increases renal excretion of prostaglandin E and water in essential fatty acid deficient rats. Lipids, 16(11), 849-854. https://doi.org/10.1007/BF02535041

Vancouver

Hansen HS. Essential fatty acid supplemented diet increases renal excretion of prostaglandin E and water in essential fatty acid deficient rats. Lipids. 1981 Nov 1;16(11):849-854. https://doi.org/10.1007/BF02535041

Author

Hansen, Harald S. / Essential fatty acid supplemented diet increases renal excretion of prostaglandin E and water in essential fatty acid deficient rats. In: Lipids. 1981 ; Vol. 16, No. 11. pp. 849-854.

Bibtex

@article{e977651c203149428d702f1f32d80728,
title = "Essential fatty acid supplemented diet increases renal excretion of prostaglandin E and water in essential fatty acid deficient rats",
abstract = "Weanling male rats were fed an essential fatty acid (EFA)-deficient diet for 25 weeks and then switched to an EFA-supplemented diet for 3 weeks. Control rats received the EFA-supplemented diet for 25 weeks and then the EFA-deficient diet for 3 weeks. Throughout the last 19 weeks, the rats were housed in metabolic cages once a week for a 24-hr period. Urinary excretion of prostaglandin E (PGE) was estimated by radioimmunoassay. Throughout a period of 12 weeks (weeks 13-24) water consumption increased ca. 60%, and urine output and PGE excretion decreased ca. 45% and 70%, respectively, in the EFA-deficient rats. Feeding EFA-supplemented diet to the EFA-deficient rats for 3 weeks decreased the water consumption and raised the urine output to that observed in the controls. However, the urine output was corrected within 1 day whereas the water consumption was not corrected until the second measurement 8 days after the dietary change. The PGE excretion increased more than 9-fold (from 18±8 ng/24 hr to 165±51 ng/24 hr) 1 day after EFA-supplementation, followed by a decrease to 86±29 ng/24 hr over the following 2 weeks. On the basis of the present data, it is suggested that EFA deficiency in rats causes diminished PGE excretion, which can be normalized by EFA supplementation. The normalization of the urine flow may, in part, be caused by the concomitant considerable increase in endogenous PGE synthesis.",
author = "Hansen, {Harald S.}",
year = "1981",
month = nov,
day = "1",
doi = "10.1007/BF02535041",
language = "English",
volume = "16",
pages = "849--854",
journal = "Lipids",
issn = "0024-4201",
publisher = "Springer",
number = "11",

}

RIS

TY - JOUR

T1 - Essential fatty acid supplemented diet increases renal excretion of prostaglandin E and water in essential fatty acid deficient rats

AU - Hansen, Harald S.

PY - 1981/11/1

Y1 - 1981/11/1

N2 - Weanling male rats were fed an essential fatty acid (EFA)-deficient diet for 25 weeks and then switched to an EFA-supplemented diet for 3 weeks. Control rats received the EFA-supplemented diet for 25 weeks and then the EFA-deficient diet for 3 weeks. Throughout the last 19 weeks, the rats were housed in metabolic cages once a week for a 24-hr period. Urinary excretion of prostaglandin E (PGE) was estimated by radioimmunoassay. Throughout a period of 12 weeks (weeks 13-24) water consumption increased ca. 60%, and urine output and PGE excretion decreased ca. 45% and 70%, respectively, in the EFA-deficient rats. Feeding EFA-supplemented diet to the EFA-deficient rats for 3 weeks decreased the water consumption and raised the urine output to that observed in the controls. However, the urine output was corrected within 1 day whereas the water consumption was not corrected until the second measurement 8 days after the dietary change. The PGE excretion increased more than 9-fold (from 18±8 ng/24 hr to 165±51 ng/24 hr) 1 day after EFA-supplementation, followed by a decrease to 86±29 ng/24 hr over the following 2 weeks. On the basis of the present data, it is suggested that EFA deficiency in rats causes diminished PGE excretion, which can be normalized by EFA supplementation. The normalization of the urine flow may, in part, be caused by the concomitant considerable increase in endogenous PGE synthesis.

AB - Weanling male rats were fed an essential fatty acid (EFA)-deficient diet for 25 weeks and then switched to an EFA-supplemented diet for 3 weeks. Control rats received the EFA-supplemented diet for 25 weeks and then the EFA-deficient diet for 3 weeks. Throughout the last 19 weeks, the rats were housed in metabolic cages once a week for a 24-hr period. Urinary excretion of prostaglandin E (PGE) was estimated by radioimmunoassay. Throughout a period of 12 weeks (weeks 13-24) water consumption increased ca. 60%, and urine output and PGE excretion decreased ca. 45% and 70%, respectively, in the EFA-deficient rats. Feeding EFA-supplemented diet to the EFA-deficient rats for 3 weeks decreased the water consumption and raised the urine output to that observed in the controls. However, the urine output was corrected within 1 day whereas the water consumption was not corrected until the second measurement 8 days after the dietary change. The PGE excretion increased more than 9-fold (from 18±8 ng/24 hr to 165±51 ng/24 hr) 1 day after EFA-supplementation, followed by a decrease to 86±29 ng/24 hr over the following 2 weeks. On the basis of the present data, it is suggested that EFA deficiency in rats causes diminished PGE excretion, which can be normalized by EFA supplementation. The normalization of the urine flow may, in part, be caused by the concomitant considerable increase in endogenous PGE synthesis.

UR - http://www.scopus.com/inward/record.url?scp=0019814488&partnerID=8YFLogxK

U2 - 10.1007/BF02535041

DO - 10.1007/BF02535041

M3 - Journal article

AN - SCOPUS:0019814488

VL - 16

SP - 849

EP - 854

JO - Lipids

JF - Lipids

SN - 0024-4201

IS - 11

ER -

ID: 45561394