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Brain metabolism of nutritionally essential polyunsaturated fatty acids depends on both the diet and the liver.
Prostaglandins Leukot Essent Fatty Acids. 2007 Nov-Dec; 77(5-6):251-61.PL

Abstract

Plasma alpha-linolenic acid (alpha-LNA, 18:3n-3) and linoleic acid (LA, 18:2n-6) do not contribute significantly to the brain content of docosahexaenoic acid (DHA, 22:6n-3) or arachidonic acid (AA, 20:4n-6), respectively, and neither DHA nor AA can be synthesized de novo in vertebrate tissue. Therefore, measured rates of incorporation of circulating DHA and AA into brain exactly represent their rates of consumption by brain. Positron emission tomography (PET) has been used to show, based on this information, that the adult human brain consumes AA and DHA at rates of 17.8 and 4.6 mg/day, respectively, and that AA consumption does not change significantly with age. In unanesthetized adult rats fed an n-3 PUFA "adequate" diet containing 4.6% alpha-LNA (of total fatty acids) as its only n-3 PUFA, the rate of liver synthesis of DHA was more than sufficient to maintain brain DHA, whereas the brain's rate of DHA synthesis is very low and unable to do so. Reducing dietary alpha-LNA in the DHA-free diet led to upregulation of liver but not brain coefficients of alpha-LNA conversion to DHA and of liver expression of elongases and desaturases that catalyze this conversion. Concurrently, brain DHA loss slowed due to downregulation of several of its DHA-metabolizing enzymes. Dietary alpha-LNA deficiency also promoted accumulation of brain docosapentaenoic acid (22:5n-6), and upregulated expression of AA-metabolizing enzymes, including cytosolic and secretory phospholipases A(2) and cyclooxygenase-2. These changes, plus reduced levels of brain derived neurotrophic factor (BDNF) and cAMP response element-binding protein (CREB) in n-3 PUFA diet deficient rats, likely render their brain more vulnerable to neuropathological insults.

Authors+Show Affiliations

Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Building 9, Room 1S128, 9000 Rockville Pike, Bethesda, MD 20892, USA. sir@helix.nih.govNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Intramural

Language

eng

PubMed ID

18060754

Citation

Rapoport, Stanley I., et al. "Brain Metabolism of Nutritionally Essential Polyunsaturated Fatty Acids Depends On Both the Diet and the Liver." Prostaglandins, Leukotrienes, and Essential Fatty Acids, vol. 77, no. 5-6, 2007, pp. 251-61.
Rapoport SI, Rao JS, Igarashi M. Brain metabolism of nutritionally essential polyunsaturated fatty acids depends on both the diet and the liver. Prostaglandins Leukot Essent Fatty Acids. 2007;77(5-6):251-61.
Rapoport, S. I., Rao, J. S., & Igarashi, M. (2007). Brain metabolism of nutritionally essential polyunsaturated fatty acids depends on both the diet and the liver. Prostaglandins, Leukotrienes, and Essential Fatty Acids, 77(5-6), 251-61.
Rapoport SI, Rao JS, Igarashi M. Brain Metabolism of Nutritionally Essential Polyunsaturated Fatty Acids Depends On Both the Diet and the Liver. Prostaglandins Leukot Essent Fatty Acids. 2007 Nov-Dec;77(5-6):251-61. PubMed PMID: 18060754.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Brain metabolism of nutritionally essential polyunsaturated fatty acids depends on both the diet and the liver. AU - Rapoport,Stanley I, AU - Rao,Jagadeesh S, AU - Igarashi,Miki, Y1 - 2007/12/03/ PY - 2007/12/7/pubmed PY - 2008/4/24/medline PY - 2007/12/7/entrez SP - 251 EP - 61 JF - Prostaglandins, leukotrienes, and essential fatty acids JO - Prostaglandins Leukot Essent Fatty Acids VL - 77 IS - 5-6 N2 - Plasma alpha-linolenic acid (alpha-LNA, 18:3n-3) and linoleic acid (LA, 18:2n-6) do not contribute significantly to the brain content of docosahexaenoic acid (DHA, 22:6n-3) or arachidonic acid (AA, 20:4n-6), respectively, and neither DHA nor AA can be synthesized de novo in vertebrate tissue. Therefore, measured rates of incorporation of circulating DHA and AA into brain exactly represent their rates of consumption by brain. Positron emission tomography (PET) has been used to show, based on this information, that the adult human brain consumes AA and DHA at rates of 17.8 and 4.6 mg/day, respectively, and that AA consumption does not change significantly with age. In unanesthetized adult rats fed an n-3 PUFA "adequate" diet containing 4.6% alpha-LNA (of total fatty acids) as its only n-3 PUFA, the rate of liver synthesis of DHA was more than sufficient to maintain brain DHA, whereas the brain's rate of DHA synthesis is very low and unable to do so. Reducing dietary alpha-LNA in the DHA-free diet led to upregulation of liver but not brain coefficients of alpha-LNA conversion to DHA and of liver expression of elongases and desaturases that catalyze this conversion. Concurrently, brain DHA loss slowed due to downregulation of several of its DHA-metabolizing enzymes. Dietary alpha-LNA deficiency also promoted accumulation of brain docosapentaenoic acid (22:5n-6), and upregulated expression of AA-metabolizing enzymes, including cytosolic and secretory phospholipases A(2) and cyclooxygenase-2. These changes, plus reduced levels of brain derived neurotrophic factor (BDNF) and cAMP response element-binding protein (CREB) in n-3 PUFA diet deficient rats, likely render their brain more vulnerable to neuropathological insults. SN - 0952-3278 UR - https://www.unboundmedicine.com/medline/citation/18060754/Brain_metabolism_of_nutritionally_essential_polyunsaturated_fatty_acids_depends_on_both_the_diet_and_the_liver_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0952-3278(07)00155-X DB - PRIME DP - Unbound Medicine ER -