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JournalISSN: 0952-3278

Prostaglandins Leukotrienes and Essential Fatty Acids 

Elsevier BV
About: Prostaglandins Leukotrienes and Essential Fatty Acids is an academic journal published by Elsevier BV. The journal publishes majorly in the area(s): Polyunsaturated fatty acid & Arachidonic acid. It has an ISSN identifier of 0952-3278. Over the lifetime, 3630 publications have been published receiving 107944 citations. The journal is also known as: PLEFA.


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Journal ArticleDOI
TL;DR: The DHA status of infants and adults consuming preformed DHA in their diets is, on average, greater than that of people who do not consume DHA, but not with supplementation of ALA, EPA, or other precursors.
Abstract: Blood levels of polyunsaturated fatty acids (PUFA) are considered biomarkers of status. Alpha-linolenic acid, ALA, the plant omega-3, is the dietary precursor for the long-chain omega-3 PUFA eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and docosahexaenoic acid (DHA). Studies in normal healthy adults consuming western diets, which are rich in linoleic acid (LA), show that supplemental ALA raises EPA and DPA status in the blood and in breast milk. However, ALA or EPA dietary supplements have little effect on blood or breast milk DHA levels, whereas consumption of preformed DHA is effective in raising blood DHA levels. Addition of ALA to the diets of formula-fed infants does raise DHA, but no level of ALA tested raises DHA to levels achievable with preformed DHA at intakes similar to typical human milk DHA supply. The DHA status of infants and adults consuming preformed DHA in their diets is, on average, greater than that of people who do not consume DHA. With no other changes in diet, improvement of blood DHA status can be achieved with dietary supplements of preformed DHA, but not with supplementation of ALA, EPA, or other precursors.

779 citations

Journal ArticleDOI
TL;DR: All together these experiments strongly suggest the possibility to modulate the plasticity of the adipose organ with therapeutic implications for obesity and related disorders.
Abstract: In mammals, the adipose tissues are contained in a multi-depot organ: the adipose organ. It consists of several subcutaneous and visceral depots. Some areas of these depots are brown and correspond to brown adipose tissue, while many are white and correspond to white adipose tissue. The organ is rich of vessels and parenchymal nerve fibers, but their density is higher in the brown areas. White areas contain a variable amount of brown adipocytes and their number varies with age, strain and environmental conditions. All adipocytes of the adipose organ express a specific adrenoceptor: ss3AR. Recent data have stressed the plasticity of the adipose organ in adult animals, and in parallel with the cytological variations there are also vascular as well as neural variations. Of note, treatment of genetically and diet induced obese rats with ss3 adrenoceptor agonists ameliorate their pathological condition and this is accompanied by the appearance of brown adipocytes in white areas of the adipose organ. This drug-induced modification of the anatomy of the organ is also obtained by the treatment with PPARgamma agonists in rats and dogs. We have previously shown that the transformation of white adipose tissue into brown adipose tissue in rats treated with ss3 adrenoceptor agonists is due to a direct transformation of differentiated unilocular adipocytes (transdifferentiation). We recently also showed that the absence of ss3 adrenoceptors strongly depress this type of plasticity in the adipose organ. All together these experiments strongly suggest the possibility to modulate the plasticity of the adipose organ with therapeutic implications for obesity and related disorders.

706 citations

Journal ArticleDOI
TL;DR: The effects of ketone body metabolism suggests that mild ketosis may offer therapeutic potential in a variety of different common and rare disease states, and current ketogenic diets are all characterized by elevations of free fatty acids, which may lead to metabolic inefficiency by activation of the PPAR system and its associated uncoupled mitochondrial uncoupling proteins.
Abstract: The effects of ketone body metabolism suggests that mild ketosis may offer therapeutic potential in a variety of different common and rare disease states. These inferences follow directly from the metabolic effects of ketosis and the higher inherent energy present in d-beta-hydroxybutyrate relative to pyruvate, the normal mitochondrial fuel produced by glycolysis leading to an increase in the DeltaG' of ATP hydrolysis. The large categories of disease for which ketones may have therapeutic effects are:(1)diseases of substrate insufficiency or insulin resistance,(2)diseases resulting from free radical damage,(3)disease resulting from hypoxia. Current ketogenic diets are all characterized by elevations of free fatty acids, which may lead to metabolic inefficiency by activation of the PPAR system and its associated uncoupling mitochondrial uncoupling proteins. New diets comprised of ketone bodies themselves or their esters may obviate this present difficulty.

612 citations

Journal ArticleDOI
TL;DR: The anti-inflammatory actions of long chain n-3 fatty acid-induced effects may be of therapeutic use in conditions with an acute or chronic inflammatory component.
Abstract: The n-6 polyunsaturated fatty acid arachidonic acid gives rise to the eicosanoid family of mediators (prostaglandins, thromboxanes, leukotrienes and related metabolites). These have inflammatory actions in their own right and also regulate the production of other mediators including inflammatory cytokines. Consumption of long chain n-3 polyunsaturated fatty acids decreases the amount of arachidonic acid in cell membranes and so available for eicosanoid production. Thus, n-3 polyunsaturated fatty acids decrease production of arachidonic acid-derived eicosanoids. These fatty acids also decrease the production of the classic inflammatory cytokines tumour necrosis factor, interleukin-1, and interleukin-6 and the expression of adhesion molecules involved in inflammatory interactions between leukocytes and endothelial cells. These latter effects may occur by eicosanoid-independent mechanisms including modulation of the activation of transcription factors involved in inflammatory processes. The anti-inflammatory actions of long chain n-3 fatty acid-induced effects may be of therapeutic use in conditions with an acute or chronic inflammatory component.

539 citations

Journal ArticleDOI
TL;DR: The principle omega-3 fatty acid in brain, docosahexaenoic acid (DHA), accumulates in the brain during perinatal cortical expansion and maturation as mentioned in this paper.
Abstract: The principle omega-3 fatty acid in brain, docosahexaenoic acid (DHA), accumulates in the brain during perinatal cortical expansion and maturation. Animal studies have demonstrated that reductions in perinatal brain DHA accrual are associated with deficits in neuronal arborization, multiple indices of synaptic pathology including deficits in serotonin and mesocorticolimbic dopamine neurotransmission, neurocognitive deficits, and elevated behavioral indices of anxiety, aggression, and depression. In primates and humans, preterm delivery is associated with deficits in fetal cortical DHA accrual, and children/adolescents born preterm exhibit deficits in cortical gray matter maturation, neurocognitive deficits particularly in the realm of attention, and increased risk for attention-deficit/hyperactivity disorder (ADHD) and schizophrenia. Individuals diagnosed with ADHD or schizophrenia exhibit deficits in cortical gray matter maturation, and medications found to be efficacious in the treatment of these disorders increase cortical and striatal dopamine neurotransmission. These associations in conjunction with intervention trials showing enhanced cortical visual acuity and cognitive outcomes in preterm and term infants fed DHA, suggest that perinatal deficits in brain DHA accrual may represent a preventable neurodevelopmental risk factor for the subsequent emergence of psychopathology.

499 citations

Performance
Metrics
No. of papers from the Journal in previous years
YearPapers
202326
202261
202174
202085
201955
201877