Altered brain lipid composition in cyclooxygenase-2 knockout mouse

Ma, Kaizong; Langenbach, Robert; Rapoport, Stanley I.; Basselin, Mireille

doi:10.1194/jlr.m600400-jlr200

Cited by 23 publications

(24 citation statements)

References 54 publications

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“…The cortical, cerebellar, hippocampal, and remainder of brain total phospholipid and phospholipid fraction esterified fatty acid as well as cholesterol concentrations from wild-type mice in this study are consistent with other reports [22,23,53,56] and slight discrepancies may be due to differences in diet and brain region analysis [1,57]. Although the majority of fatty acids were not statistically different, small decreases in monounsaturated fatty acids were detected in total phospholipids and the major phospholipid classes of CD36 -/-mice.…”

Section: Discussionsupporting

confidence: 89%

“…The fatty acid percentage compositions of the mouse diet, as measured by gas chromatography, were as follows: 16:0, 15.2%; 18:0, 3.5%; 18:1n-9, 19.6%; 18:2n-6, 51.8%; 18:3n-3, 5.6%; and fatty acids longer than 20 carbons accounted for less than 1% of total fatty acids. By 9 weeks of age, mice have an intact BBB [52], an adult size brain [21], and plateaued brain PUFA concentrations [53,54]. Hence, mice were euthanized at 9 weeks of age with carbon dioxide and the cortex, cerebellum, hippocampus, and remainder of the brain were extracted.…”

Section: Animals and Treatmentsmentioning

confidence: 99%

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Genetic Ablation of CD36 Does not Alter Mouse Brain Polyunsaturated Fatty Acid Concentrations

Song

Elbert

Rahman

et al. 2010

Lipids

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In the brain, polyunsaturated fatty acids (PUFA), especially arachidonic acid and docosahexaenoic acid (DHA), are required for regulating membrane fluidity, neuronal survival and signal transduction. Since the brain cannot synthesize n-6 and n-3 PUFA de novo, they must be supplied from the blood. However, the methods of PUFA entry into the brain are not agreed upon. This study tested the necessity of CD36, a candidate transporter of unesterified fatty acids, for maintaining brain PUFA concentrations by comparing brain PUFA concentrations in CD36(-/-) mice to their wild-type littermates. Because CD36(-/-) mice have been reported to have impaired learning ability, the PUFA concentrations in different brain regions (cortex, hippocampus, cerebellum and the remainder of brain) were investigated. At 9 weeks of age, the brain was separated into the four regions and fatty acid concentrations in total and phospholipid classes of these brain regions were analyzed using thin layer and gas chromatography. There were no statistical differences in arachidonic acid or DHA concentrations in the different brain regions between wild-type and CD36(-/-) mice, in total or phospholipid fractions. Concentrations of monounsaturated fatty acids were decreased in several phospholipid fractions in CD36(-/-) mice. These findings suggest that CD36 is not necessary for maintaining brain PUFA concentrations and that other mechanisms must exist.

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Section: Discussionsupporting

confidence: 89%

Section: Animals and Treatmentsmentioning

confidence: 99%

Genetic Ablation of CD36 Does not Alter Mouse Brain Polyunsaturated Fatty Acid Concentrations

Song

Elbert

Rahman

et al. 2010

Lipids

View full text Add to dashboard Cite

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“…The cortex and brain stem phospholipid esterified fatty acid concentrations from wild-type mice in this study are similar to literature values (45,51), and slight discrepancies are likely attributable to differences in diet and brain region analyses (1,52). 20:4n-6 from the plasma unesterified pool is rapidly esterified to ChoGpl and PtdIns (51,53), whereas 22:6n-3 is rapidly esterified to EtnGpl and ChoGpl (54,55).…”

Section: Discussionsupporting

confidence: 69%

“…The 18:2n-6 and 18:3n-3% composition of the diet (measured by gas chromatography) was 40.5% and 5.4%, respectively, and longer-chain PUFAs were not detected. We analyzed 7 week old mice because in them the blood-brain barrier is intact (42), the brain has reached its adult size (43), brain PUFA concentrations have plateaued (44,45), and the brain halflives of PUFAs in rodents are ?1 month (46,47). At 7 weeks of age, mice were subjected to head-focused high-intensity microwave irradiation (6 kW, 0.88-0.91 s; Muromachi brain fixation system; Stoelting Co., Chicago, IL) to stop brain fatty acid metabolism (48,49).…”

Section: Methodsmentioning

confidence: 99%

The low density lipoprotein receptor is not necessary for maintaining mouse brain polyunsaturated fatty acid concentrations

Chen

W.L.

Kim

et al. 2008

Journal of Lipid Research

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The brain cannot synthesize n-6 or n-3 PUFAs de novo and requires their transport from the blood. Two models of brain fatty acid uptake have been proposed. One requires the passive diffusion of unesterified fatty acids through endothelial cells of the blood-brain barrier, and the other requires the uptake of lipoproteins via a lipoprotein receptor on the luminal membrane of endothelial cells. This study tested whether the low density lipoprotein receptor (LDLr) is necessary for maintaining brain PUFA concentrations. Because the cortex has a low basal expression of LDLr and the anterior brain stem has a relatively high expression, we analyzed these regions separately. LDLr knockout (LDLr 2/2 ) and wild-type mice consumed an AIN-93G diet ad libitum until 7 weeks of age. After microwaving, the cortex and anterior brain stem (pons and medulla) were isolated for phospholipid fatty acid analyses. There were no differences in phosphatidylserine, phosphatidylinositol, ethanolamine, or choline glycerophospholipid esterified PUFA or saturated or monounsaturated fatty acid concentrations in the cortex or brain stem between LDLr 2/2 and wild-type mice. These findings demonstrate that the LDLr is not necessary for maintaining brain PUFA concentrations and suggest that other mechanisms to transport PUFAs into the brain must

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“…Absorbance was read at 797 nm. Phospholipid concentrations were determined using standard curves as described (Ma, Langenbach, Rapoport, & Basselin, 2007). …”

Section: Methodsmentioning

confidence: 99%

Brain lipid concentrations in bipolar disorder

Igarashi

Gao

et al. 2010

Journal of Psychiatric Research

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Reduced concentrations of docosahexaenoic acid (DHA, and arachidonic acid (AA,) have been reported in the postmortem bipolar disorder (BD) brain. Additionally, an increased prevalence of BD has been related to low dietary intake of fish, and dietary supplements containing fish products or DHA have been reported to ameliorate BD symptoms. These observations suggest that brain lipid metabolism, particularly involving DHA, is disturbed in BD. To test this suggestion, concentrations of different lipids were measured using internal standards in postmortem frontal cortex from eight BD patients and six matched controls. Compared with control cortex, the BD cortex showed no statistically significant difference in mean concentrations (per gram wet weight) of "stable" lipids (total lipid, total phospholipid, individual phospholipids, or cholesterol), of unesterified fatty acids, or of esterified DHA or AA within stable lipids. Fractional esterified AA and DHA concentrations also did not differ significantly between groups. Some fatty acid concentration differences were found in low-abundant cholesteryl ester. These results do not support the hypothesis of disturbed brain lipid concentrations, including concentrations of AA and DHA, in BD. Positron emission tomography might be used, however, to see if brain AA or DHA kinetics are disturbed in the disease.

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Altered brain lipid composition in cyclooxygenase-2 knockout mouse

Cited by 23 publications

References 54 publications

Genetic Ablation of CD36 Does not Alter Mouse Brain Polyunsaturated Fatty Acid Concentrations

Genetic Ablation of CD36 Does not Alter Mouse Brain Polyunsaturated Fatty Acid Concentrations

The low density lipoprotein receptor is not necessary for maintaining mouse brain polyunsaturated fatty acid concentrations

Brain lipid concentrations in bipolar disorder

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