Cholesteryl ester depletion from the ovaries of superovulated female rats fed a normal or essential fatty acid deficient diet

1978 ◽  
Vol 56 (4) ◽  
pp. 585-590 ◽  
Author(s):  
Angela K. Young ◽  
Brian L. Walker
Keyword(s):  
Fatty Acid ◽  
Cholesteryl Ester ◽  
Essential Fatty Acid ◽  
Corn Oil ◽  
Ovarian Tissue ◽  
Coconut Oil ◽  
Female Rats ◽  
Unit Mass ◽  
Deficient Diet ◽  
Cholesteryl Ester Content

The cholesteryl ester content of the ovaries was determined in rats fed diets containing corn oil or hydrogenated coconut oil (essential fatty acid (EFA) deficient) and subjected to superovulation by injection of luteinizing hormone and follicle-stimulating hormone. Superovulation increased ovarian weight; the effect was greater in animals fed corn oil. Superovulation significantly decreased total ovarian cholesteryl ester concentration in animals fed corn oil, with disproportionately large decreases occurring in the esters of 20:1, 20:2, 22:5ω6, and 22:6ω3. Significant decreases were observed in these esters when the data were expressed on a unit mass of tissue basis or in relation to total ovarian mass. In superovulated, EFA-deficient rats, esters of 18:1, 20:1, 22:5ω6, and 22:6ω3 were significantly lower per unit mass of tissue but this was due, in all cases except that of 22:6ω3, to the increased mass of ovarian tissue; there was no decrease in total esters per ovary weight during superovulation of deficient rats. The pattern and degree of selective changes in ovarian cholesteryl esters during superovulation were different from those previously reported for adrenal esters of stresssd rats.

Lipids of the intestinal mucosa of normal and essential fatty acid deficient rats

1970 ◽  
Vol 48 (9) ◽  
pp. 631-639 ◽  
Author(s):  
M. Yurkowski ◽  
B. L. Walker
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acids ◽  
Essential Fatty Acid ◽  
Corn Oil ◽  
Essential Fatty Acids ◽  
Coconut Oil ◽  
Fatty Acid Deficiency ◽  
Arachidonic Acids ◽  
Layer Chromatography

Mucosal lipids were isolated from the proximal, middle, and distal intestinal sections of rats fed diets containing either 10% corn oil or 10% hydrogenated coconut oil, the latter diet being deficient in essential fatty acids. By a combination of column and thin-layer chromatography, the lipids were fractionated and the major components found to consist of triglycerides, free fatty acids, cholesterol, phosphatidylcholine, and phosphatidylethanolamine. Several minor constituents were present. Triglycerides and free fatty acids were generally present in higher concentrations in animals fed corn oil, and the concentration of mucosal triglycerides decreased towards the distal end of the intestine whereas free fatty acids increased in this group. Essential fatty acid deficiency resulted in lower levels of linoleic and arachidonic acids and higher levels of palmitoleic, oleic, and eicosatrienoic acids in the mucosal lipids. Mono- and di-enoic fatty acids tended to decrease in concentration from the proximal to the distal end of the intestine; the polyunsaturated acids and, to some extent, the saturated acids, were lowest in the proximal section of the intestine.

scholarly journals Influence of sex and gonadal hormones on rat-liver and carcass lipids during the development of an essential fatty acid deficiency

1965 ◽  
Vol 97 (2) ◽  
pp. 485-499 ◽  
Author(s):  
R Ostwald ◽  
P Bouchard ◽  
P Miljanich ◽  
RL Lyman
Keyword(s):  
Arachidonic Acid ◽  
Fatty Acid ◽  
Linoleic Acid ◽  
Essential Fatty Acid ◽  
Essential Fatty Acid Deficiency ◽  
Eicosatrienoic Acid ◽  
Female Rats ◽  
Male Rats ◽  
Acid Deficiency ◽  
Fatty Acid Deficiency

1. Groups of intact male and female rats and castrated rats injected with oestradiol or testosterone were given a diet containing hydrogenated coconut oil for 9 weeks, and at intervals the amounts and fatty acid compositions of the carcass and liver lipids were determined. 2. Male rats grew faster and larger, and exhibited typical external essential fatty acid deficiency symptoms sooner than did females. Testosterone-treated castrated male rats were similar to males, and oestradiol-injected castrated male rats resembled females. 3. Intact females maintained a higher linoleic acid concentration in their carcass than did males. Total amounts of carcass linoleic acid remained similar for all groups, only 200mg. being removed in 9 weeks regardless of body size. 4. The amounts of total cholesteryl esters were independent of liver size. They were higher in males and testosterone-treated castrated male rats than in females and oestrogen-treated castrated male rats. 5. Phospholipids represented about 80% of the liver lipids. The total amounts of the phospholipid linoleic acid and arachidonic acid were similar for all groups regardless of liver size, and were not affected appreciably by the deficiency. Females and oestrogen-treated castrated male rats maintained a higher proportion of phospholipid arachidonic acid for longer periods than did their male counterparts. Both the total amounts and the proportions of eicosatrienoic acid and palmitic acid were higher in males than in females. 6. Supplementation of the essential fatty acid-deficient diet with linoleic acid caused a rapid loss of eicosatrienoic acid and palmitic acid with a concomitant increase in stearic acid and arachidonic acid. 7. There were no obvious differences in the way that the essential fatty acids were metabolized or mobilized from adipose tissue of male or female rats during essential fatty acid deficiency. 8. The results indicated that the greater growth rate of the male rats caused them to require and synthesize more phospholipids than did the females. In the absence of adequate amounts of arachidonic acid, eicosatrienoic acid was substituted into the additional phospholipid. The earlier symptoms of essential fatty acid deficiency in the male rat could therefore be ascribed to the higher tissue concentrations of this unnatural phospholipid and its inability to perform the normal metabolic functions of phospholipids.

Estrogen replacement stimulates fatty acid oxidation and impairs post-ischemic recovery of hearts from ovariectomized female rats

2002 ◽  
Vol 80 (10) ◽  
pp. 1001-1007 ◽  
Author(s):  
Mark Grist ◽  
Richard B Wambolt ◽  
Gregory P Bondy ◽  
Dean R English ◽  
Michael F Allard
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Corn Oil ◽  
Heart Function ◽  
Ischemia Reperfusion ◽  
Female Rats ◽  
Acid Oxidation ◽  
Estrogen Replacement ◽  
Lipid Utilization ◽  
Intact Rats

Women less than 50 years of age, the majority of whom are likely premenopausal and exposed to estrogen, are at greater risk of a poor short-term recovery after myocardial ischemia than men and older women. Since estrogen enhances non-cardiac lipid utilization and increased lipid utilization is associated with poor post-ischemic heart function, we determined the effect of estrogen replacement on post-ischemic myocardial function and fatty acid oxidation. Female Sprague–Dawley rats, either intact (n = 15) or ovariectomized and treated with 17β-estradiol (0.1 mg·kg–1·day–1, s.c., n = 14) or corn oil vehicle (n = 16) for 5 weeks, were compared. Function and fatty acid oxidation of isolated working hearts perfused with 1.2 mM [9,10-3H]palmitate, 5.5 mM glucose, 0.5 mM lactate, and 100 mU/L insulin were measured before and after global no-flow ischemia. Only 36% of hearts from estrogen-treated rats recovered after ischemia compared with 56% from vehicle-treated rats (p > 0.05, not significant), while 93% of hearts from intact rats recovered (p < 0.05). Relative to pre-ischemic values, post-ischemic function of estrogen-treated hearts (26.3 ± 10.1%) was significantly lower than vehicle-treated hearts (53.4 ± 11.8%, p < 0.05) and hearts from intact rats (81.9 ± 7.0%, p < 0.05). Following ischemia, fatty acid oxidation was greater in estrogen-treated hearts than in the other groups. Thus, estrogen replacement stimulates fatty acid oxidation and impairs post-ischemic recovery of isolated working hearts from ovariectomized female rats.Key words: fatty acid oxidation, estrogen, ischemia, reperfusion.

Sign in / Sign up

Export Citation Format

Share Document