Effect of feeding ethionine on the distribution and metabolism of 1-14C-linoleic acid in the rat

1969 ◽  
Vol 47 (1) ◽  
pp. 11-17 ◽  
Author(s):  
R. L. Lyman ◽  
C. Giotas ◽  
M. A. Fosmire ◽  
P. Miljanich

Male rats fed a 9% casein-purified diet for 14 days were compared with a similar group of rats whose diet contained 0.25% DL-ethionine. At the end of the feeding period, the animals were tube fed their respective diets plus 1-14C-linoleic acid, and control and experimental rats randomly chosen were then killed 18 h and 30 h thereafter. Composition and radioactivity were determined in carcass and liver lipids. Total amounts of carcass and liver lipids did not differ among the groups, nor were there any differences in the distribution or specific activity of the carcass linoleate. Liver triglyceride of rats fed ethionine, while being no higher in concentration than that of control animals, did, however, have a higher proportion of radioactivity and more linoleic acid with a higher specific activity than did the controls. The differences were greatest at the 18-h post-feeding period. Ethionine also increased the proportion of linoleic acid and decreased that of arachidonic acid in the liver phospholipids as compared with controls. Analysis of the phosphatidylethanolamines and phosphatidylcholines showed that by the 18-h post-feeding period, the proportions of radioactivity and specific activity of arachidonic acid in both phospholipid fractions were reduced far below control values, whereas the specific activity of linoleic acid was high and similar for all groups. However, by 30 h after administration of the labeled linoleic acid, specific activities, but not the distribution of the label, had returned to normal ranges. From the results it was concluded that the liver phospholipid fatty acid patterns seen in rats fed ethionine were a consequence of an impairment by the analogue in the normal utilization and conversion of linoleic acid to arachidonic acid.

1965 ◽  
Vol 97 (2) ◽  
pp. 485-499 ◽  
Author(s):  
R Ostwald ◽  
P Bouchard ◽  
P Miljanich ◽  
RL Lyman

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.


1964 ◽  
Vol 42 (3) ◽  
pp. 365-376 ◽  
Author(s):  
R. L. Lyman ◽  
Angela Shannon ◽  
Rosemarie Ostwald ◽  
P. Miljanich

The effects of physiological doses of estradiol and testosterone on plasma cholesteryl ester and phospholipid fatty acid composition were investigated in castrated male rats. The animals were killed after 3 weeks on experiment, and their plasma cholesteryl esters and phospholipids were analyzed and compared with those of intact female and male rats.Estradiol appeared to be responsible for the increased proportion of plasma cholesteryl arachidonate seen in the female or estrogen-injected rats since the proportion of cholesteryl arachidonate in castrated control rats was lower and similar to that of male or testosterone-treated rats. Plasma phospholipids of female and estradiol-injected rats had a higher percentage of stearic acid relative to palmitic acid. On the other hand, male, castrated control and testosterone-treated rats had higher proportions of palmitic acid. Fractionation of the plasma phospholipids into cephalins, lecithins, sphingomyelins, and lysolecithins, and analyses of their fatty acids, revealed that a principal effect of estradiol was to increase proportions and amounts of stearic and arachidonic acids in the lecithin fraction.The results suggest that estradiol may influence the synthesis of a lecithin rich in stearic and arachidonic acid. A possible relationship between the arachidonic-acid-rich lecithin and the higher percentage of cholesteryl arachidonate in estradiol-treated rats is discussed.


1988 ◽  
Vol 59 (2) ◽  
pp. 273-278 ◽  
Author(s):  
Stephen C. Cunnane

1. Young male rats were fed on diets containing 3·4, 36 or 411 mg zinc/kg for 10 weeks in order to determine whether effects of Zn deficiency on plasma and liver essential fatty acid composition could be distinguished from those of reduced protein and energy intake.2. Fatty acid analysis revealed that a Zn intake of 3·4 mg/kg (plasma Zn 0·80 v. 1·97 mmol/l in controls fed on 36 mg Zn/kg) resulted in a significant increase in the linoleic acid: arachidonic acid ratio in both plasma and liver phospholipids in comparison with rats fed on 36 or 411 mg Zn/kg.3. Zn supplementation (411 mg/kg) decreased the linoleic acid: arachidonic acid ratio in plasma phosphatidylserine compared with that of the controls.4. The previously reported increase in arachidonic acid (mol %) in liver triacylglycerol of Zn-deficient rats was shown to be a function of a reduced liver triacylglycerol pool size; quantitatively, triacylglycerol content of arachidonic acid in the liver was not significantly affected by Zn intake.


2016 ◽  
Vol 46 (2) ◽  
pp. 190-203 ◽  
Author(s):  
Sherazede Bouderbala ◽  
Malika Bouchenak

Purpose – The purpose of this study is to compare the effect of olive or salmon oil on the hepatic storage and transport of fatty acids by very-low-density lipoproteins (VLDL). Design/methodology/approach – In all, 24 male Wistar rats (80 ± 5 g) were fed a 0.5 per cent cholesterol-enriched diet with either 20 per cent casein (C) or chickpea (CP) proteins with 10 per cent olive (O) or salmon (S) oil for 28 days. Findings – In VLDL-triacyglycerols fatty acids, oleic acid content was higher in CPS as compared to that in CS or CPO and lower in CS and CPO than that in CO; linoleic acid content was higher in all groups; arachidonic acid content was higher in CS and CPO as compared to that in CO. In the liver, TG fatty acids content was lower in CPO or CPS as compared to that in CO or CS; oleic and arachidonic acid contents were lower in CPS than that in CPO; linoleic acid content was lower in CS, CPS and CPO than that in CO, CPO and CO. In liver, phospholipid fatty acid, oleic and arachidonic acid contents were lower in CPS than that in CS; oleic, linoleic and arachidonic acid contents were lower in CPO compared to that in CO. In liver, cholesteryl esters fatty acids, oleic, linoleic and arachidonic acids contents were higher in CPS as compared to that in CS; oleic, linoleic and arachidonic acid contents were lower in CS as compared to that in CO; linoleic and arachidonic acid contents were lower in CPS than that in CPO. Originality/value – A cholesterol-enriched diet containing casein or chickpea proteins combined with olive or salmon oil affects the hepatic storage and transport of polyunsaturated and monounsaturated fatty acids by VLDL.


1985 ◽  
Vol 249 (1) ◽  
pp. F12-F19 ◽  
Author(s):  
B. A. Molitoris ◽  
A. C. Alfrey ◽  
R. A. Harris ◽  
F. R. Simon

Renal proximal tubule cells adapt to dietary phosphate (Pi) restriction by increasing Pi transport independent of parathyroid hormone, vitamin D metabolites, or serum Ca2+. To determine the underlying cellular mechanism(s), brush border (BBM) and basolateral membranes (BLM) were isolated from growing male rats fed a synthetic diet containing variable levels of Pi (0.1-1.4%). Dietary Pi restriction was without effect on either BBM or BLM total lipid phosphorus, individual phospholipid species, or BLM Na+-K+-ATPase specific activity. However, dietary Pi restriction (0.1 vs. 1.0%) did cause a significant reduction in BBM but not BLM cholesterol (0.45 vs. 0.41 mumol/mg protein). Brush border membrane cholesterol was inversely correlated with the tubular reabsorption of Pi (r = 0.77, P less than 0.01) over a broad range (99.9-46.2%). Arrhenius analysis of two intrinsic BBM enzymes revealed a significant reduction in the breakpoint temperature for alkaline phosphatase but no change for Mg2+-ATPase. Fluorescence polarization studies showed increased BBM inner core fluidity due to an alteration in neutral lipids but not phospholipid, fatty acid, or protein membrane components. These data demonstrate that the BBM can regulate its cholesterol content independent of the BLM. Furthermore, they suggest that adaptation to dietary Pi restriction involves a reduction in BBM cholesterol, which may be mediated by an increase in membrane fluidity.


1967 ◽  
Vol 105 (1) ◽  
pp. 343-350 ◽  
Author(s):  
R. R. Johnson ◽  
P. Bouchard ◽  
J. Tinoco ◽  
R. L. Lyman

1. Fatty acid patterns of liver and plasma triglycerides, phospholipids and cholesteryl esters were determined at intervals during 24hr. after essential fatty acid-deficient rats were given one feeding of linoleate (as safflower oil). 2. Liver triglyceride, phospholipid and cholesteryl ester fatty acid compositions did not change up to 7hr. after feeding. Between 7 and 10hr., linoleic acid began to increase in all fractions, but arachidonic acid did not begin to rise in the phospholipid until 14–19hr. after feeding. 3. Oleic acid and eicosatrienoic acid in liver phospholipid began to decline at about the time that linoleic acid increased, i.e. about 9hr. before arachidonic acid began to increase. 4. Changes in linoleic acid, arachidonic acid and eicosatrienoic acid in phosphatidylcholine resembled those of the total phospholipid. Phosphatidylethanolamine had a higher percentage content of arachidonic acid before the linoleate was given than did phosphatidylcholine, and after the linoleate was given the fatty acid composition of this fraction was little changed. 5. The behaviour of the plasma lipid fatty acids was similar to that of the liver lipids, with changes in linoleic acid, eicosatrienoic acid and arachidonic acid appearing at the same times as they occurred in the liver. 6. The results indicated that linoleic acid was preferentially incorporated into the liver phospholipid at the expense of eicosatrienoic acid and oleic acid. The decline in these fatty acids apparently resulted from their competition with linoleic acid for available sites in the phospholipids rather than from any direct replacement by arachidonic acid.


Sign in / Sign up

Export Citation Format

Share Document