docosapentaenoic-acid and Vitamin-A-Deficiency

The synthesis of docosahexaenoic (DHA, 22:6n-3) and Osbond acid (OA, 22:5n-6) is regulated by the heterodimer of peroxisome proliferator-activated receptor and retinoid X receptor (RXR). 9-Cis retinoic acid, a metabolite of vitamin A, is the most potent ligand of RXR. We tested whether vitamin A deficiency impairs DHA and OA synthesis in rats fed a vitamin A- and alpha-linolenic acid (ALA)-sufficient (VASALAS), vitamin A-sufficient and ALA-deficient (VASALAD), vitamin A-deficient and ALA-sufficient (VADALAS), or vitamin A- and ALA-deficient (VADALAD) diet. After 7 wk of feeding, liver and colon choline (CPG) and ethanolamine (EPG) phosphoglyceride FA were analyzed. The VADALAS compared with the VASALAS rats had elevated levels of both DHA (P< 0.05) and OA (P < 0.005) in liver CPG and EPG. In contrast, the VADALAD group had a lower DHA (P < 0.01) and higher OA (P < 0.005) level in CPG and EPG of both tissues than their VASALAD counterparts. ALA deficiency reduced DHA and enhariced OA levels in liver and colon CPG and EPG in both the vitamin A-sufficient (VASALAS vs. VASALAD) and -deficient (VADALAS vs. VADALAD) rats (P < 0.005). The study demonstrates that ALA deficiency reduced DHA and enhanced OA levels in tissue membranes, and dietary vitamin A deficiency has a profound effect on membrane DHA and OA in rat tissues. Both vitamin A and DHA are involved in a myriad of vital physiological functions pertaining to growth and development and health. Hence, there is a need for a further study to unravel the mechanism by which vitamin A influences membrane DHA and OA.

Topics: alpha-Linolenic Acid; Animals; Colon; Dietary Fats, Unsaturated; Docosahexaenoic Acids; Eating; Fatty Acids, Unsaturated; Intra-Abdominal Fat; Liver; Male; Phosphatidylcholines; Phosphatidylethanolamines; Rats; Rats, Wistar; Vitamin A; Vitamin A Deficiency; Weight Gain

Weanling albino rats were fed a vitamin-A-adequate diet or vitamin-A-deficient diet and maintained in a cyclic light or dark environment for up to 14 weeks. One half of the rats were supplemented with additional dietary linolenic acid in the form of linseed oil. The lipid composition and rhodopsin-opsin contents of isolated rod outer segments were determined after 6-7 weeks or 12-14 weeks on diet. This study shows that feeding rats a standard vitamin A-adequate or -deficient diet results in an age-dependent loss of omega three docosahexaenoic acid and a concomitant increase in omega six docosapentanoic acid in the rod outer segments. The loss of docosahexaenoate appears to be caused by insufficient dietary omega three fatty acids. The increase in omega six docosapentanoic acid appears to arise from the high concentration of linoleic acid in standard diets containing either cottonseed, or peanut oil or supplemental corn oil. Feeding rats diets supplemented with linseed oil, however, results in a rod outer-segment lipid profile which is the same as for chow-fed animals. The same effects were seen in the fatty-acid profile of lipids from liver, although the content of polyunsaturates was much lower than in rod outer segments. Vitamin A deficiency, itself, does not lead to changes in the fatty-acid composition of either the rod outer segments or liver. After 6-7 weeks on A+ or A- diet, rhodopsin levels were, as expected, higher in dark-reared rats than in cyclic-light animals. Although the rhodopsin levels in dark-reared vitamin A-adequate rats were significantly higher than in vitamin A-deficient animals, measurements of the lipid to opsin ratio of rod outer segments indicate that the rods of vitamin A-deficient rats are not markedly different than those of vitamin A-adequate rats. It is concluded that these diets may be useful in providing a means for evaluating the role of docosahexaenoic acid in visual cell death from damaging light.

Topics: Age Factors; Animals; Docosahexaenoic Acids; Eye Proteins; Fatty Acids; Fatty Acids, Unsaturated; Linolenic Acids; Lipid Metabolism; Liver; Male; Photoreceptor Cells; Rats; Rats, Inbred Strains; Rhodopsin; Rod Cell Outer Segment; Rod Opsins; Vitamin A; Vitamin A Deficiency