Metabolism of Gamma-Linolenic Acid in Essential Fatty Acid-deficient Rats

1977 ◽  
Vol 107 (4) ◽  
pp. 519-524 ◽  
Author(s):  
Ahmed G. Hassam ◽  
John P. W. Rivers ◽  
Michael A. Crawford
1990 ◽  
Vol 28 (18) ◽  
pp. 69-70

Epogam capsules (Scotia) contain oil from the seed of the evening primrose which is rich in the essential fatty acid linoleic acid and its metabolite gamolenic (gamma-linolenic) acid. Epogam is licensed for use to relieve symptoms in atopic eczema, and is claimed to act at a fundamental metabolic level in this disease. Conventional treatment of eczema is often unsatisfactory, and any claim of an advance must be taken seriously. How well founded are the claims made for Epogam?


1996 ◽  
Vol 271 (3) ◽  
pp. E471-E476 ◽  
Author(s):  
N. E. Cameron ◽  
M. A. Cotter

Nerve conduction and perfusion deficits in diabetic rats depend on increased oxidative stress and impaired n-6 essential fatty acid metabolism, which are corrected by free radical scavenger and gamma-linolenic acid (GLA)-rich oil treatments, respectively. We investigated the interaction between these mechanisms on conduction velocity and endoneurial blood flow by use of low-dose antioxidant (BM15.0639) and GLA treatments, alone and in combination. After 8 wk of streptozotocin-induced diabetes, sciatic motor conduction velocity was 20.9% reduced. Treatment with GLA or BM15.0639 for the final 2 wk corrected this deficit by 18.5 and 20.0%, respectively; however, joint treatment caused 71.5% improvement, corresponding to a 7.5-fold amplification of individual drug effects. A 48.3% deficit in sciatic nutritive endoneurial blood flow was corrected by 34.8 and 24.8% with GLA and BM15.0639 treatments, respectively. With joint treatment, the flow improvement of 72.5% was greater than expected from individual drug effects, indicating a facilitatory interaction. Thus the synergistic effect of combined antioxidant and n-6 essential fatty acid treatment could potentially provide increased therapeutic power against diabetic neuropathy.


1977 ◽  
Vol 38 (1) ◽  
pp. 137-140 ◽  
Author(s):  
A. G. Hassam

1.Essential fatty acid-deficient rats were fed γ-linolenic acid (18:3ω6) at 2 % dietary energy and α-linolenic acid (18:3ω3) at 0, 1.6, 2.8 and 4.0 % of the dietary energy.2.18:3ω3 at 1.6% apparently inhibits the synthesis of the C20 and C22 ω6 long-chain polyunsaturated fatty acids (ω6 LC-PUFA) metabolized from 18:3ω6.3.However, increasing the dietary levels of 18:3ω3 from 1.6 to 4.0% has no further influence.4.The results suggest that dietary 18:3ω6 is an efficient precursor for the ω6 LC-PUFA synthesis even in the presence of 18:3ω3.


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