scholarly journals The effect of essential-fatty-acid deficiency on the activity of liver phosphatidate phosphatase in rats

1981 ◽  
Vol 198 (2) ◽  
pp. 413-416 ◽  
Author(s):  
James H. Stewart ◽  
George M. Briggs

The activities of the soluble and microsomal phosphatidate phosphatases (EC 3.1.3.4) are greater in the livers of essential-fatty-acid-deficient rats than in rats fed diets containing linoleic 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.


1980 ◽  
Vol 238 (5) ◽  
pp. E499-E505 ◽  
Author(s):  
M. T. Huang ◽  
M. A. Williams

Hepatic triglyceride secretion in essential fatty acid-deficient rats was examined by three separate techniques in an effort to resolve conflicting evidence on the question of whether essential fatty acid deficiency altered hepatic triglyceride secretion in vivo. First, plasma triglyceride turnover was measured by intravenous injection of [2-3H]glycerol trioleate. Equations of the kinetics were formulated based on a single, open pool model. Turnover rates and pool sizes of plasma triglyceride were calculated from these equations. Second, [2-3H]glycerol was injected, and apparent rate constants for plasma triglyceride secretion and clearance were calculated by kinetic analysis. Third, Triton WR-1339 was used to inhibit lipoprotein clearance from blood plasma, and rates of plasma triglyceride accumulation were measured. The results of these studies showed that the rate of hepatic triglyceride secretion was 2-3 times greater in essential fatty acid-deficient rats than in nondeficient controls. The increase in triglyceride secretion, as well as the higher level of liver triglyceride typical of essential fatty acid-deficient rats, could be caused by increased lipogenesis and increased mobilization of fatty acids from adipose tissues.


Author(s):  
Asim Maqbool ◽  
Joan I. Schall ◽  
Babette S. Zemel ◽  
J. Felipe Garcia-Espana ◽  
Birgitta Strandvik ◽  
...  

2000 ◽  
Vol 279 (6) ◽  
pp. G1242-G1248 ◽  
Author(s):  
Deanna M. Minich ◽  
Rick Havinga ◽  
Frans Stellaard ◽  
Roel J. Vonk ◽  
Folkert Kuipers ◽  
...  

We investigated in bile duct-ligated (BDL) and sham-operated control rats whether the frequent presence of essential fatty acid deficiency in cholestatic liver disease could be related to linoleic acid malabsorption, altered linoleic acid metabolism, or both. In plasma of BDL rats, the triene-to-tetraene ratio, a biochemical marker for essential fatty acid deficiency, was increased compared with controls (0.024 ± 0.004 vs. 0.013 ± 0.001; P < 0.05). Net and percentage of dietary linoleic acid absorbed were decreased in BDL rats compared with control rats (1.50 ± 0.16 mmol/day and 81.3 ± 3.3% vs. 2.08 ± 0.07 mmol/day and 99.2 ± 0.1%, respectively; each P < 0.001). At 24 h after [13C]linoleic acid administration, BDL rats had a similar ratio of plasma [13C]arachidonic acid to plasma [13C]linoleic acid concentration compared with control rats. Δ6-Desaturase activity was not significantly different in hepatic microsomes from control or BDL rats. At 3 h after [13C]linoleic acid administration, plasma appearance of [13C]linoleic acid and cumulative expiration of 13CO2 were decreased in BDL rats, compared with controls (by 54% and 80%, respectively). The present data indicate that the impaired linoleic acid status in cholestatic liver disease is mainly due to decreased net absorption and not to quantitative alterations in postabsorptive metabolism.


1990 ◽  
Vol 79 (4) ◽  
pp. 299-305 ◽  
Author(s):  
L. Hjelte ◽  
M. Larsson ◽  
A. Alvestrand ◽  
A.-S. Malmborg ◽  
B. Strandvik

1. Renal function was studied in 50-, 70-, 90- and 200-day-old rats with essential fatty acid deficiency. The pharmacokinetics of tobramycin was investigated in 90-day-old essential fatty acid-deficient rats. 2. A higher glomerular filtration rate and a higher serum concentration of urea were seen in 50-day-old essential fatty acid-deficient rats compared with age-matched controls. Later, the glomerular filtration rate progressively deteriorated in parallel with a decline in effective renal plasma flow and with a concomittant rise in serum levels of urea and creatinine. The serum concentration of protein was lower in the rats with essential fatty acid deficiency and that of sodium was higher than in the control rats. The non-renal clearance of tobramycin was increased in the rats with essential fatty acid deficiency. 3. The early hyperfiltration in essential fatty acid-deficient rats with the subsequent fall in glomerular filtration rate, which was paralleled by a rise in serum levels of urea and creatinine, as well as the increased non-renal clearance of tobramycin, are in accordance with the clinical manifestations of cystic fibrosis. Rats with essential fatty acid deficiency might be a useful model with which to study the pathophysiological renal changes in cystic fibrosis related to the progressive essential fatty acid deficiency in this disease.


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