PMID- 18060754
OWN - NLM
STAT- MEDLINE
DCOM- 20080423
LR  - 20231105
IS  - 0952-3278 (Print)
IS  - 0952-3278 (Linking)
VI  - 77
IP  - 5-6
DP  - 2007 Nov-Dec
TI  - Brain metabolism of nutritionally essential polyunsaturated fatty acids depends 
      on both the diet and the liver.
PG  - 251-61
AB  - 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.
FAU - Rapoport, Stanley I
AU  - Rapoport SI
AD  - 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.gov
FAU - Rao, Jagadeesh S
AU  - Rao JS
FAU - Igarashi, Miki
AU  - Igarashi M
LA  - eng
GR  - Z99 AG999999/ImNIH/Intramural NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Intramural
DEP - 20071203
PL  - Scotland
TA  - Prostaglandins Leukot Essent Fatty Acids
JT  - Prostaglandins, leukotrienes, and essential fatty acids
JID - 8802730
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (Dietary Fats)
RN  - 0 (Fatty Acids, Essential)
RN  - 0 (Fatty Acids, Omega-3)
RN  - 0 (Fatty Acids, Unsaturated)
RN  - 0 (Phospholipids)
RN  - 25167-62-8 (Docosahexaenoic Acids)
SB  - IM
MH  - Animals
MH  - Brain/*metabolism
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Cyclic AMP Response Element-Binding Protein/metabolism
MH  - Dietary Fats/administration & dosage/*metabolism
MH  - Docosahexaenoic Acids/metabolism
MH  - Fatty Acids, Essential/*metabolism
MH  - Fatty Acids, Omega-3/metabolism
MH  - Fatty Acids, Unsaturated/*metabolism
MH  - Humans
MH  - Liver/*metabolism
MH  - Models, Biological
MH  - Phospholipids/metabolism
MH  - Rats
PMC - PMC2725409
MID - NIHMS36609
EDAT- 2007/12/07 09:00
MHDA- 2008/04/24 09:00
PMCR- 2009/08/12
CRDT- 2007/12/07 09:00
PHST- 2007/12/07 09:00 [pubmed]
PHST- 2008/04/24 09:00 [medline]
PHST- 2007/12/07 09:00 [entrez]
PHST- 2009/08/12 00:00 [pmc-release]
AID - S0952-3278(07)00155-X [pii]
AID - 10.1016/j.plefa.2007.10.023 [doi]
PST - ppublish
SO  - Prostaglandins Leukot Essent Fatty Acids. 2007 Nov-Dec;77(5-6):251-61. doi: 
      10.1016/j.plefa.2007.10.023. Epub 2007 Dec 3.