PubMed haku anta 19 vastausta , josita tuoreimmat otan sitaattina 25.5. 2016.
Dyall SC, Mandhair HK, Fincham RE, Kerr DM, Roche M, Molina-Holgado F.
Neuropharmacology. 2016 Apr 1;107:387-395. doi: 10.1016/j.neuropharm.2016.03.055. [Epub ahead of print]
Emerging evidence suggests a complex interplay between the endocannabinoid system, omega-3 fatty acids and the immune system in the promotion of brain self-repair. However, it is unknown if all omega-3 fatty acids elicit similar effects on adult neurogenesis and if such effects are mediated or regulated by interactions with the endocannabinoid system. This study investigated the effects of DHA and EPA on neural stem cell (NSC) fate and the role of the endocannabinoid
signalling pathways in these effects.
EPA, but not DHA, significantly
increased proliferation of NSCs compared to controls, an effect
associated with enhanced levels of the endocannabinoid
2-arachidonylglycerol (2-AG) and p-p38 MAPK, effects attenuated by
pre-treatment with CB1 (AM251) or CB2 (AM630) receptor antagonists.
Furthermore, in NSCs derived from IL-1β deficient mice, EPA
significantly decreased proliferation and p-p38 MAPK levels compared to
controls, suggesting a key role for IL-1β signalling in the effects
observed. Although DHA similarly increased 2-AG levels in wild-type
NSCs, there was no concomitant increase in proliferation or p-p38 MAPK
activity.
In addition, in NSCs from IL-1β deficient mice, DHA
significantly increased proliferation without effects on p-P38 MAPK,
suggesting effects of DHA are mediated via alternative signalling
pathways.
These results provide crucial new insights into the divergent
effects of EPA and DHA in regulating NSC proliferation and the pathways
involved, and highlight the therapeutic potential of their interplay
with endocannabinoid signalling in brain repair.
2.
Simopoulos AP.
Nutrients. 2016 Mar 2;8(3). pii: E128. doi: 10.3390/nu8030128. Review.
In the past three decades, total fat and saturated fat intake as a
percentage of total calories has continuously decreased in Western
diets, while the intake of omega-6 fatty acid increased and the omega-3 fatty acid
decreased, resulting in a large increase in the omega-6/omega-3 ratio
from 1:1 during evolution to 20:1 today or even higher. This change in
the composition of fatty acids
parallels a significant increase in the prevalence of overweight and
obesity. Experimental studies have suggested that omega-6 and omega-3
fatty acids
elicit divergent effects on body fat gain through mechanisms of
adipogenesis, browning of adipose tissue, lipid homeostasis,
brain-gut-adipose tissue axis, and most importantly systemic
inflammation. Prospective studies clearly show an increase in the risk
of obesity as the level of omega-6 fatty acids
and the omega-6/omega-3 ratio increase in red blood cell (RBC) membrane
phospholipids, whereas high omega-3 RBC membrane phospholipids decrease
the risk of obesity. Recent studies in humans show that in addition to
absolute amounts of omega-6 and omega-3 fatty acid
intake, the omega-6/omega-3 ratio plays an important role in increasing
the development of obesity via both AA eicosanoid metabolites and
hyperactivity of the cannabinoid system, which can be reversed with increased intake of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). A balanced omega-6/omega-3 ratio is important for health and in the prevention and management of obesity.
3.
Adibfar A, Saleem M, Lanctot KL, Herrmann N.
Curr Mol Med. 2016;16(2):137-64.
Depression,
the most common mood disorder, is a leading contributor to the global
burden of disease affecting more than 120 million individuals worldwide.
Various pathophysiological processes underlie depression; this
complexity renders it difficult to identify clinically useful diagnostic
and prognostic markers, as well as treatment options. The current state
of knowledge driving the management and treatment of depression remains
incomplete, which underscores the need for further insight into
pathways relevant to depression. Exploring co-morbid conditions, such as
coronary artery disease, may be useful to further elucidate the
etiopathology of depression. The present review therefore systematically
identifies and critically evaluates relevant markers of depression as
assessed in a high-risk population, namely patients with coronary artery
disease. Biomarkers related to hypothalamicpituitary- adrenal axis
dysregulation, inflammation, endothelial dysfunction, platelet
activation and aggregation, serotonin activity, sympathetic nervous system
activation, thyroid function, structural and morphological brain
abnormalities, genetic variation, lipid metabolism, one-carbon
metabolism, endocannabinoid
signalling irregularities, and vitamin D deficiency are reviewed.
Markers exhibiting the most consistent associations with depression
include tumour necrosis factor-α, flow-mediated dilation, endothelin-1,
endothelial progenitor cells, brain-derived neurotrophic factor, and docosahexaenoic acid.
Further investigating the mechanisms underlying those markers and
exploring novel pathways, such as oxidative stress, will extend the
current state of knowledge and potentially lead to the identification of
novel therapeutic targets.
4.
Kim J, Carlson ME, Kuchel GA, Newman JW, Watkins BA.
Int J Obes (Lond). 2016 Jan;40(1):129-37. doi: 10.1038/ijo.2015.135. Epub 2015 Jul 29.
5.
Naughton SS, Mathai ML, Hryciw DH, McAinch AJ.
Int J Endocrinol. 2013;2013:361895. doi: 10.1155/2013/361895. Epub 2013 May 26.
Endocannabinoids and their G-protein coupled receptors (GPCR) are a current research focus in the area of obesity due to the system's
role in food intake and glucose and lipid metabolism.
Importantly,
overweight and obese individuals often have higher circulating levels of
the arachidonic acid-derived endocannabinoids
anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) and an altered
pattern of receptor expression. Consequently, this leads to an increase
in orexigenic stimuli, changes in fatty acid synthesis, insulin sensitivity, and glucose utilisation, with preferential energy storage in adipose tissue
. As endocannabinoids are products of dietary fats, modification of dietary intake may modulate their levels, with eicosapentaenoic and docosahexaenoic acid based endocannabinoids being able to displace arachidonic acid from cell membranes, reducing AEA and 2-AG production. Similarly, oleoyl ethanolamide, a product of oleic acid, induces satiety, decreases circulating fatty acid
concentrations, increases the capacity for β -oxidation, and is capable
of inhibiting the action of AEA and 2-AG in adipose tissue. Thus,
understanding how dietary fats alter endocannabinoid system
activity is a pertinent area of research due to public health messages
promoting a shift towards plant-derived fats, which are rich sources of
AEA and 2-AG precursor fatty acids, possibly encouraging excessive energy intake and weight gain.
6.
Meijerink J, Balvers M, Witkamp R.
Br J Pharmacol. 2013 Jun;169(4):772-83. doi: 10.1111/bph.12030. Review.
N-3 Long-chain polyunsaturated fatty acids (n-3 LC-PUFAs), in particular α-linolenic acid (18:3n-3), eicosapentaenoic acid (EPA; 20:5n-3) and docosahexaenoic acid
(DHA; 22:6n-3) are receiving much attention because of their presumed
beneficial health effects. To explain these, a variety of mechanisms
have been proposed, but their interactions with the endocannabinoid system
have received relatively little attention so far. However, it has
already been shown some time ago that consumption of n-3 LC-PUFAs not
only affects the synthesis of prototypic endocannabinoids
like anandamide but also stimulates the formation of specific n-3
LC-PUFA-derived conjugates with ethanolamine, dopamine, serotonin or
other amines. Some of these fatty amides show overlapping biological
activities with those of typical endocannabinoids,
whereas others possess distinct and sometimes largely unknown receptor
affinities and other properties. The ethanolamine and dopamine
conjugates of DHA have been the most investigated thus far. These
mediators may provide promising new leads to the field of inflammatory
and neurological disorders and for other pharmacological applications,
including their use as carrier molecules for neurotransmitters to target
the brain. Furthermore, combinations of n-3 LC-PUFA-derived fatty acid amides, their precursors and FAAH inhibitors offer possibilities to optimise their effects in health and disease.Free PMC Article
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