Fatty Acids and Brain Peptides

Yehuda, Shlomo; Rabinovitz, Sharon; Carasso, R; Mostofsky, David I.

doi:10.1016/s0196-9781(97)00295-7

Cited by 62 publications

(38 citation statements)

References 139 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Neuronal activities in IL rats infused with etomoxir were normalised in ARC, LH, PVN and VMH, as assessed by c-fos immunostaining, and the effect of NEFA on GIIS and hepatic insulin sensitivity was blunted. This is consistent with the results of some studies indicating that NEFA may alter the synthesis or the release of neuropeptides [25]. The effect of a NEFA overload could be partially mediated by an increase in ATP production, which could inactivate ATP-sensitive K + channels and trigger cell exocytosis.…”

Section: Discussionsupporting

confidence: 92%

Beta oxidation in the brain is required for the effects of non-esterified fatty acids on glucose-induced insulin secretion in rats

Cruciani-Guglielmacci

Hervalet

Douared

et al. 2004

Diabetologia

View full text Add to dashboard Cite

show abstract

Section: Discussionsupporting

confidence: 92%

Beta oxidation in the brain is required for the effects of non-esterified fatty acids on glucose-induced insulin secretion in rats

Cruciani-Guglielmacci

Hervalet

Douared

et al. 2004

Diabetologia

View full text Add to dashboard Cite

show abstract

“…We have recently reviewed the complex relationships between simple EFAs and complex lipids, such as cholesterol, and various brain neurotransmitters releasing factors and hormones, and essential amino acids (Yehuda et al, 1998). Figure 1 describes the effects of essentialamino acids and immune factors on brain mediated cognitive (e.g., learning), and physiological (e.g., pain, sleep, and thermoregulation) functions.…”

Section: Essential Fatty Acids and Essential Amino Acidsmentioning

confidence: 99%

Essential fatty acids are mediators of brain biochemistry and cognitive functions

1999

Self Cite

View full text Add to dashboard Cite

Major advances have been made in understanding the biochemistry of essential fatty acids (FA) and their interactions with metabolic pathways leading to the production of longer and more complex fatty acids and lipids. Less understood are the roles played by FA which are known to affect neurotransmitters, peptides, releasing factors, hormones, and a variety of physiological and cognitive processes. Based on empirical findings we propose that (a) FA exert a controlling function in the modulation of neuronal membrane fluidity, and (b) the critical factor in FA action and efficacy is not absolute level but rather the ratio between various groups of FA. This approach unifies the biochemical and cognitive results obtained from many different and unrelated fields of research.

show abstract

“…The present finding is consistent with studies (4,29,30) that have shown that dietary DHA competes with 20:4n-6, the main n-6 PUFA, for incorporation into brain PL classes, and restores the ratio between n-6 PUFA and n-3 PUFA of brain PL classes. Studies have indicated that the ratio of the dietary intake of n-6 and n-3 PUFA has a determining influence on the level of performance in learning and memory tasks (43)(44)(45). The improved acquisition and retention of T-maze foot-shock avoidance, demonstrated in the present study, could be related to the lower ratio between n-6 PUFA and n-3 PUFA found in the brain PL classes of the SAMP8 mice induced by the high-DHA diet.…”

Section: Discussionmentioning

confidence: 99%

Morley's “A Brief History of Geriatrics”

Achenbaum¹

2004

The Journals of Gerontology: Series A

View full text Add to dashboard Cite

Animal studies have shown that a deficiency in brain of the n-3 polyunsaturated fatty acid (PUFA) docosahexaenoic acid (DHA) is associated with memory loss and diminished cognitive function. The senescence-accelerated prone 8 (SAMP8) mouse develops impairments in learning and memory at 8-12 months of age. The effect of diet supplemented with n-3 PUFA on brain phospholipid DHA status, learning, and memory ability in aged SAMP8 mice was investigated. At the age of 10 months, SAMP8 mice were fed either a low-DHA or a high-DHA diet for 8 weeks. In comparison to SAMP8 mice fed the low-DHA diet, those fed a high-DHA diet had improved acquisition and retention in a T-maze foot shock avoidance test and a higher proportion of DHA in hippocampal and amygdala phospholipids. This study demonstrates that, in mature animals, DHA is incorporated into brain phospholipids and that dietary n-3 PUFA is associated with delay in cognitive decline.Key Words: Alzheimer's disease-n-3 Polyunsaturated fatty acids-Docosahexaenoic acid-Hippocampus-Memory. BRAIN tissue membrane phospholipids (PL) are rich in the n-3 polyunsaturated fatty acid (PUFA) docosahexaenoic acid . It has been shown that the balance between DHA and the n-6 PUFA arachidonic acid (20:4n-6) in brain membrane PL is crucial for normal functioning of the central nervous system (1-5). Humans and animals must obtain essential n-3 PUFA and n-6 PUFA from their diet. The sources for DHA and 20:4n-6 in brain membrane PL are derived from the diet or from conversion of their respective dietary precursors in liver (6,7). The precursors of DHA are a-linolenic acid from plant products and eicosapentaenoic acid (EPA or 20:5n-3) of marine origin and that of 20:4n-6 is linoleic acid (18:2n-6).Studies demonstrate that lipid peroxidation in brain is an early event in Alzheimer's disease (AD), which strengthens the hypothesis that oxidative damage may play a role in the pathogenesis of AD (8,9). The double bonds in PUFA are highly susceptible to peroxidative damage, which is initiated by reactive oxygen species (10) and results in a decrease in content of n-6 PUFA and n-3 PUFA in membrane PL. Decrease in the DHA content of hippocampal tissue during aging has been demonstrated in patients with AD (11) and in 12-month-old senescence-accelerated prone 8 (SAMP8) mice (12). The SAMP8 strain of mice is a model of AD, because the mice develop age-related deficits in learning and memory that is associated with an age-related overexpression of amyloid precursor protein (APP) and elevated levels of amyloid-beta (Ab) protein in brain (13-18). According to the amyloid hypothesis, accumulation of Ab protein is central to the pathogenesis of . It has been suggested that DHA is a possible therapeutic agent for ameliorating learning deficiencies caused by AD, which could act by suppressing the increases in the levels of lipid peroxide, reactive oxygen species, and amyloid accumulation in AD models (22)(23)(24).Epidemiological (25)(26)(27) and animal studies (28-31) have reported that there is an associati...

show abstract

Fatty Acids and Brain Peptides

Cited by 62 publications

References 139 publications

Beta oxidation in the brain is required for the effects of non-esterified fatty acids on glucose-induced insulin secretion in rats

Beta oxidation in the brain is required for the effects of non-esterified fatty acids on glucose-induced insulin secretion in rats

Essential fatty acids are mediators of brain biochemistry and cognitive functions

Morley's “A Brief History of Geriatrics”

Contact Info

Product

Resources

About