Effect of docosahexaenoic acid supplementation on retinal function in a patient with autosomal dominant Stargardt-like retinal dystrophy.
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Adolescent↗
Biomedical subjects
J Jumpsen
Publications and source records attributed to J Jumpsen.
Small changes of dietary (n-6) and (n-3)/fatty acid content ration alter phosphatidylethanolamine and phosphatidylcholine fatty acid composition during development of neuronal and glial cells in rats.
It has been suggested that the fat composition of infant formula should provide arachidonic acid [20:4(n-6)] and docosahexaenoic acid [22:6(n-3)] or increased alpha-linolenic acid [18:3(n-3)] to optimize the (n-3) and (n-6) fatty acid content of brain during infant development. This experiment examined the effects of feeding increased levels of 18:3(n-3), 20:4(n-6) and 22:6(n-3) on brain development in neonatal rats. Diets varying in (n-6) and (n-3) fatty acid content with or without 20:4(n-6) or 22:6(n-3), at levels proposed for infant formula, were fed to nursing dams from parturition and subsequently to weaned pups until 6 wk of age. Neuronal and glial cells were isolated from the frontal region, cerebellum and hippocampus of the brain. Fatty acid analyses of ethanolamine- and choline-phosphoglycerides indicated that small changes in the dietary (n-6)/(n-3) ratio significantly altered neuronal and glial membrane fatty acid composition. Brain regions and cell types varied in amount and rate of 20:4(n-6) and 22:6(n-3) accretion. Fatty acid composition of individual phosphoglycerides was distinct and exhibited changes with age. Inclusion of both 20:4(n-6) and 22:6(n-3) in the diet resulted in alteration of brain fatty acid composition reflecting the fatty acid composition of the diet. If analogous developmental changes occur in human brain, then these results imply that addition of 20:4(n-6) and 22:6(n-3) or a reduced 18:2(n-6):18:3(n-3) ratio in infant formula may result in fatty acid profiles of neuronal and glial cells in formula-fed infants similar to those observed in breast-fed infants.
Aging↗
Relationship between fatty acid accretion, membrane composition, and biologic functions.
Dietary fat affects metabolic pathways for phospholipid biosynthesis in tissues in a coordinated fashion. This may be important to aspects of development that concern phosphatidylcholine metabolism or regulatory processes that depend on signals from a changing milieu in the microenvironment of the membrane. Dietary fat influences the phosphatidylethanolamine (PE) composition in many membranes of the brain and retina and may by altered by small changes in the content of 20:4(6) and 22:6(3). Membrane PE fatty acids that contain one, four, or six double bonds and the ratio of 22:5(6) to 22:6(3) in PE that contains four to six double bonds are also affected. An increase in the omega 6 fatty acid content of membranes is associated with increased PE methyltransferase activity and decreased phosphocholine transferase activity, thus indicating a mechanism by which change in an exogenous factor (e.g., dietary fat intake) may alter neural phospholipid biosynthesis. Small changes in the composition of dietary fat intake change the composition of brain membranes during development. It is provocative to ponder whether diet could be used to induce formation of membrane structures that are more resistant to specific insults that cause degeneration of brain structural material, to ensure optimal functional compositions, or to reverse degenerative changes that occur in neural membrane structure and function.
Animals↗