Document Detail


Essential fatty acid deficiency delays the onset of puberty in the female rat.
MedLine Citation:
PMID:  2759037     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This study assessed the effect of a dietary deficiency in the essential fatty acids (EFA) linoleic and linolenic acids on the onset of female puberty. EFA deficiency was produced in female rats by means of a semipurified diet and was biochemically documented by analyzing serum and erythrocyte fatty acid levels of more than 30 fatty acids, including all members of the n-6 and n-3 series. Levels of linoleic acid (18:2 n-6) and all n-6 derivatives, particularly arachidonic acid, were strikingly reduced. A less pronounced but clear-cut decrease in n-3 fatty acids, including docosahexaenoic acid (22:6 n-3) was also found. The times of puberty and first ovulation, as assessed by the ages at vaginal opening and first diestrus, were significantly delayed in EFA-deficient rats. The mechanisms underlying this delay appear to reside at both hypothalamic and ovarian sites. Simulation of preovulatory plasma estradiol (E2) levels via implantation of E2-containing Silastic capsules evoked a LH surge 30 h later in control juvenile rats, but not in EFA-deficient animals, indicating a delay in the development of the hypothalamic component of E2-positive feedback in the latter group. This delay appears to be due at least in part to reduced prostaglandin E2 (PGE2) synthesis, as the ability of the neurotransmitter norepinephrine to induce PGE2 release from median eminence nerve terminals was markedly reduced in EFA-deficient rats compared with that in controls. The decrease in hypothalamic PGE2 release was related to the EFA deficiency and not to reduced PG synthase activity, as determined by HPLC analysis of PG synthase products derived from exogenous [14C]arachidonic acid. Basal and hCG-stimulated PGE2 synthesis was also compromised in ovaries from EFA-deficient rats. Depressed gonadal function resulting from the EFA deficiency was further evidenced by a reduced gonadotropin receptor content, a blunted E2 response to hCG in vitro, and an increase in mean serum FSH levels. These results suggest that the delay in puberty resulting from EFA deficiency is due to a reduced availability of arachidonic acid for synthesis of bioactive metabolites. This results in delayed development of both the hypothalamic and ovarian components of the reproductive axis.
Authors:
S S Smith; M Neuringer; S R Ojeda
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Endocrinology     Volume:  125     ISSN:  0013-7227     ISO Abbreviation:  Endocrinology     Publication Date:  1989 Sep 
Date Detail:
Created Date:  1989-09-20     Completed Date:  1989-09-20     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1650-9     Citation Subset:  AIM; IM    
Affiliation:
Department of Anatomy, Hahnemann University, Philadelphia, Pennsylvania 19102-1192.
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MeSH Terms
Descriptor/Qualifier:
Animals
Body Weight
Dietary Fats / pharmacology
Erythrocytes / analysis
Estradiol / biosynthesis,  pharmacology
Fatty Acids / blood
Fatty Acids, Essential / deficiency*
Female
Luteinizing Hormone / blood,  secretion
Median Eminence / metabolism
Ovary / metabolism
Pituitary Hormones, Anterior / blood
Pregnancy
Progesterone / biosynthesis
Prostaglandins / biosynthesis
Rats
Rats, Inbred Strains
Reference Values
Sexual Maturation* / drug effects
Grant Support
ID/Acronym/Agency:
5T32-HD-07062/HD/NICHD NIH HHS; HD-09988-PROJECT IV/HD/NICHD NIH HHS; RR-00163/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Dietary Fats; 0/Fatty Acids; 0/Fatty Acids, Essential; 0/Pituitary Hormones, Anterior; 0/Prostaglandins; 50-28-2/Estradiol; 57-83-0/Progesterone; 9002-67-9/Luteinizing Hormone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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