Fifteen weeks of dietary n-3 polyunsaturated fatty acid deprivation increase turnover of n-6 docosapentaenoic acid in rat-brain phospholipids

Igarashi, Miki; Kim, Hyung‐Wook; Gao, Fei; Chang, Lisa; Ma, Kaizong; Rapoport, Stanley I.

doi:10.1016/j.bbalip.2011.11.002

Cited by 18 publications

(15 citation statements)

References 76 publications

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“…We and others have previously shown that increased brain content of DPA n-6, together with reduced brain DHA content, is associated with behavioral impairment in adult rodents fed with diet deprived of n-3 PUFAs (Lim et al, 2005a;Mingam et al, 2008;Lafourcade et al, 2011;Igarashi et al, 2012;Larrieu et al, 2012;Moranis et al, 2012;Larrieu et al, 2014). Of note, in all these studies, n-3 PUFA deficiency started early in life, covering the in utero and lactation period.…”

Section: )mentioning

confidence: 90%

Dietary n-3 PUFAs Deficiency Increases Vulnerability to Inflammation-Induced Spatial Memory Impairment

Delpech

Thomazeau

Madore

et al. 2015

Neuropsychopharmacol

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Dietary n-3 polyunsaturated fatty acids (PUFAs) are critical components of inflammatory response and memory impairment. However, the mechanisms underlying the sensitizing effects of low n-3 PUFAs in the brain for the development of memory impairment following inflammation are still poorly understood. In this study, we examined how a 2-month n-3 PUFAs deficiency from pre-puberty to adulthood could increase vulnerability to the effect of inflammatory event on spatial memory in mice. Mice were given diets balanced or deficient in n-3 PUFAs for a 2-month period starting at post-natal day 21, followed by a peripheral administration of lipopolysaccharide (LPS), a bacterial endotoxin, at adulthood. We first showed that spatial memory performance was altered after LPS challenge only in n-3 PUFA-deficient mice that displayed lower n-3/n-6 PUFA ratio in the hippocampus. Importantly, long-term depression (LTD), but not long-term potentiation (LTP) was impaired in the hippocampus of LPS-treated n-3 PUFA-deficient mice. Proinflammatory cytokine levels were increased in the plasma of both n-3 PUFA-deficient and n-3 PUFA-balanced mice. However, only n-3 PUFA-balanced mice showed an increase in cytokine expression in the hippocampus in response to LPS. In addition, n-3 PUFA-deficient mice displayed higher glucocorticoid levels in response to LPS as compared with n-3 PUFA-balanced mice. These results indicate a role for n-3 PUFA imbalance in the sensitization of the hippocampal synaptic plasticity to inflammatory stimuli, which is likely to contribute to spatial memory impairment.

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Section: )mentioning

confidence: 90%

Dietary n-3 PUFAs Deficiency Increases Vulnerability to Inflammation-Induced Spatial Memory Impairment

Delpech

Thomazeau

Madore

et al. 2015

Neuropsychopharmacol

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“…As noted in the Introduction, K* represents combined diffusional and enzymatic steps involved in DHA incorporation from plasma into brain phospholipid, replacing the DHA that has been metabolically lost [18], [20], [21]. K* was increased when plasma DHA concentration was reduced by severe (three generations) or moderate (12 weeks in one generation) dietary n-3 PUFA restriction in rats [12], [44]. Although we did not detect a lower plasma DHA concentration in the alcoholics at the scan time, with their typically poor dietary habits and frequent liver dysfunction, chronic alcoholics often have reduced plasma concentrations [45].…”

Section: Discussionmentioning

confidence: 99%

Brain Docosahexaenoic Acid [DHA] Incorporation and Blood Flow Are Increased in Chronic Alcoholics: A Positron Emission Tomography Study Corrected for Cerebral Atrophy

et al. 2013

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ObjectiveChronic alcohol dependence has been associated with disturbed behavior, cerebral atrophy and a low plasma concentration of docosahexaenoic acid (DHA, 22∶6n-3), particularly if liver disease is present. In animal models, excessive alcohol consumption is reported to reduce brain DHA concentration, suggesting disturbed brain DHA metabolism. We hypothesized that brain DHA metabolism also is abnormal in chronic alcoholics.MethodsWe compared 15 non-smoking chronic alcoholics, studied within 7 days of their last drink, with 22 non-smoking healthy controls. Using published neuroimaging methods with positron emission tomography (PET), we measured regional coefficients (K*) and rates (Jin) of DHA incorporation from plasma into the brain of each group using [1-11C]DHA, and regional cerebral blood flow (rCBF) using [15O]water. Data were partial volume error corrected for brain atrophy. Plasma unesterified DHA concentration also was quantified.ResultsMean K* for DHA was significantly and widely elevated by 10–20%, and rCBF was elevated by 7%–34%, in alcoholics compared with controls. Unesterified plasma DHA did not differ significantly between groups nor did whole brain Jin, the product of K* and unesterified plasma DHA concentration.DiscussionSignificantly higher values of K* for DHA in alcoholics indicate increased brain avidity for DHA, thus a brain DHA metabolic deficit vis-à-vis plasma DHA availability. Higher rCBF in alcoholics suggests increased energy consumption. These changes may reflect a hypermetabolic state related to early alcohol withdrawal, or a general brain metabolic change in chronic alcoholics.

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“…Females were mated with normal-chow fed males and placed on diets adequate (ADQ) or deficient (DEF) in n-3 PUFAs (Dyets Inc., Bethlehem, PA) (32–35). First generation (G1) rats were weaned at post-natal day (PND) 21, and males were tested on behavioral tasks.…”

Section: Methodsmentioning

confidence: 99%

Adolescent Behavior and Dopamine Availability Are Uniquely Sensitive to Dietary Omega-3 Fatty Acid Deficiency

Bondi

Taha

Tock

et al. 2014

Biological Psychiatry

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Background Understanding the nature of environmental factors that contribute to behavioral health is critical for successful prevention strategies in individuals at-risk for psychiatric disorders. These factors are typically experiential in nature, such as stress and urbanicity, but nutrition, in particular dietary deficiency of omega-3 polyunsaturated fatty acids (n-3 PUFAs), has increasingly been implicated in the symptomatic onset of schizophrenia and mood disorders, which typically occurs during adolescence to early adulthood. Thus, adolescence may be the critical age range for the negative impact of diet as an environmental insult. Methods A rat model involving consecutive generations of n-3 PUFA deficiency was developed based on the assumption that dietary trends toward decreased consumption of these fats began four-five decades ago when the parents of current adolescents were born. Behavioral performance in a wide range of tasks, as well as markers of dopamine-related neurotransmission was compared in adolescents and adults fed n-3 PUFA adequate and deficient diets. Results In adolescents, dietary n-3 PUFA deficiency across consecutive generations produced a modality-selective and task-dependent impairment in cognitive and motivated behavior distinct from the deficits observed in adults. While this dietary deficiency affected expression of dopamine-related proteins in both age groups, in adolescents, but not adults, there was an increase in tyrosine hydroxylase expression that was selective to the dorsal striatum. Conclusions These data support a nutritional contribution to optimal cognitive and affective functioning in adolescents. Furthermore, they suggest that n-3 PUFA deficiency disrupts adolescent behaviors through enhanced dorsal striatal dopamine availability.

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Fifteen weeks of dietary n-3 polyunsaturated fatty acid deprivation increase turnover of n-6 docosapentaenoic acid in rat-brain phospholipids

Cited by 18 publications

References 76 publications

Dietary n-3 PUFAs Deficiency Increases Vulnerability to Inflammation-Induced Spatial Memory Impairment

Dietary n-3 PUFAs Deficiency Increases Vulnerability to Inflammation-Induced Spatial Memory Impairment

Brain Docosahexaenoic Acid [DHA] Incorporation and Blood Flow Are Increased in Chronic Alcoholics: A Positron Emission Tomography Study Corrected for Cerebral Atrophy

Adolescent Behavior and Dopamine Availability Are Uniquely Sensitive to Dietary Omega-3 Fatty Acid Deficiency

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