scholarly journals DHA and EPA Content and Fatty Acid Profile of 39 Food Fishes from India

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Bimal Prasanna Mohanty ◽  
Satabdi Ganguly ◽  
Arabinda Mahanty ◽  
T. V. Sankar ◽  
R. Anandan ◽  
...  

Docosahexaenoic acid (DHA) is the principal constituent of a variety of cells especially the brain neurons and retinal cells and plays important role in fetal brain development, development of motor skills, and visual acuity in infants, lipid metabolism, and cognitive support and along with eicosapentaenoic acid (EPA) it plays important role in preventing atherosclerosis, dementia, rheumatoid arthritis, Alzheimer’s disease, and so forth. Being an essential nutrient, it is to be obtained through diet and therefore searching for affordable sources of theseω-3 polyunsaturated fatty acids (PUFA) is important for consumer guidance and dietary counseling. Fish is an important source of PUFA and has unique advantage that there are many food fish species available and consumers have a wide choice owing to availability and affordability. The Indian subcontinent harbors a rich fish biodiversity which markedly varies in their nutrient composition. Here we report the DHA and EPA content and fatty acid profile of 39 important food fishes (including finfishes, shellfishes, and edible molluscs from both marine water and freshwater) from India. The study showed that fishesTenualosa ilisha,Sardinella longiceps,Nemipterus japonicus, andAnabas testudineusare rich sources of DHA and EPA. Promotion of these species as DHA rich species would enhance their utility in public health nutrition.

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Huban Thomas Rajarethnem ◽  
Kumar Megur Ramakrishna Bhat ◽  
Malsawmzuali Jc ◽  
Siva Kumar Gopalkrishnan ◽  
Ramesh Babu Mugundhu Gopalram ◽  
...  

Choline is an essential nutrient for humans which plays an important role in structural integrity and signaling functions. Docosahexaenoic acid (DHA) is a polyunsaturated fatty acid, highly enriched in cell membranes of the brain. Dietary intake of choline or DHA alone by pregnant mothers directly affects fetal brain development and function. But no studies show the efficacy of combined supplementation of choline and DHA on fetal neurodevelopment. The aim of the present study was to analyze fetal neurodevelopment on combined supplementation of pregnant dams with choline and DHA. Pregnant dams were divided into five groups: normal control [NC], saline control [SC], choline [C], DHA, and C + DHA. Saline, choline, and DHA were given as supplements to appropriate groups of dams. NC dams were undisturbed during entire gestation. On postnatal day (PND) 40, brains were processed for Cresyl staining. Pups from choline or DHA supplemented group showed significant (p<0.05) increase in number of neurons in hippocampus when compared to the same in NC and SC groups. Moreover, pups from C + DHA supplemented group showed significantly higher number of neurons (p<0.001) in hippocampus when compared to the same in NC and SC groups. Thus combined supplementation of choline and DHA during normal pregnancy enhances fetal hippocampal neurodevelopment better than supplementation of choline or DHA alone.


2017 ◽  
Vol 39 (1) ◽  
pp. 26-29
Author(s):  
Dilys J. Freeman ◽  
Barbara J. Meyer

How does a mother supply a key building block of the brain required for neurodevelopment to her fetus in pregnancy? The critical requirement of docosahexaenoic acid (DHA) for fetal brain development, and the poor efficiency of its synthesis in humans, is a tricky metabolic problem to be overcome in pregnant women. Supplying this unique fatty acid to the fetus requires exquisite specificity and timing, processes that can unravel in disease conditions such as pre-eclampsia.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Colleen P. E. Rollins ◽  
Jane R. Garrison ◽  
Maite Arribas ◽  
Aida Seyedsalehi ◽  
Zhi Li ◽  
...  

Abstract All perception is a construction of the brain from sensory input. Our first perceptions begin during gestation, making fetal brain development fundamental to how we experience a diverse world. Hallucinations are percepts without origin in physical reality that occur in health and disease. Despite longstanding research on the brain structures supporting hallucinations and on perinatal contributions to the pathophysiology of schizophrenia, what links these two distinct lines of research remains unclear. Sulcal patterns derived from structural magnetic resonance (MR) images can provide a proxy in adulthood for early brain development. We studied two independent datasets of patients with schizophrenia who underwent clinical assessment and 3T MR imaging from the United Kingdom and Shanghai, China (n = 181 combined) and 63 healthy controls from Shanghai. Participants were stratified into those with (n = 79 UK; n = 22 Shanghai) and without (n = 43 UK; n = 37 Shanghai) hallucinations from the PANSS P3 scores for hallucinatory behaviour. We quantified the length, depth, and asymmetry indices of the paracingulate and superior temporal sulci (PCS, STS), which have previously been associated with hallucinations in schizophrenia, and constructed cortical folding covariance matrices organized by large-scale functional networks. In both ethnic groups, we demonstrated a significantly shorter left PCS in patients with hallucinations compared to those without, and to healthy controls. Reduced PCS length and STS depth corresponded to focal deviations in their geometry and to significantly increased covariance within and between areas of the salience and auditory networks. The discovery of neurodevelopmental alterations contributing to hallucinations establishes testable models for these enigmatic, sometimes highly distressing, perceptions and provides mechanistic insight into the pathological consequences of prenatal origins.


2013 ◽  
Vol 11 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Koshiro Nishikuni ◽  
Guilherme Carvalhal Ribas

Object The surface of the developing fetal brain undergoes significant morphological changes during fetal growth. The purpose of this study was to evaluate the morphological development of the brain sulci from the fetal to the early postnatal period. Methods Two hundred fourteen brain hemispheres from 107 human brain specimens were examined to evaluate the timing of sulcal formation, from its appearance to its complete development. These brains were obtained from cadavers ranging in age from 12 weeks of gestation to 8 months of postnatal life. Results The order of appearance of the cerebral sulci, and the number and percentages of specimens found in this study were as follows: longitudinal cerebral fissure at 12 weeks (10/10, 100%); callosal sulcus at 12 weeks (10/10, 100%); hippocampal sulcus at 15 weeks (7/10, 70%); lateral sulcus at 17 weeks (20/22, 90.9%); circular insular sulcus at 17 weeks (18/22, 81.8%); olfactory sulcus at 17 weeks (18/22, 81.8%); calcarine sulcus at 17 weeks (14/22, 63.6%); parietooccipital sulcus at 17 weeks (11/22, 50%); cingulate sulcus at 19 weeks (16/20, 80%); central sulcus at 21 weeks (22/38, 57.9%); orbital sulcus at 22 weeks (9/16, 56.2%); lunate sulcus at 24 ± 2 weeks (12/16, 75%); collateral sulcus at 24 ± 2 weeks (8/16, 50%); superior frontal sulcus at 25 ± 2 weeks (5/6, 83.3%); rhinal sulcus at 25 ± 2 weeks (3/6, 50%); precentral sulcus at 26 ± 3 weeks (2/4, 50%); postcentral sulcus at 26 ± 3 weeks (2/4, 50%); superior temporal sulcus at 26 ± 3 weeks (2/4, 50%); central insular sulcus at 29 ± 2 weeks (4/4, 100%); intraparietal sulcus at 29 ± 2 weeks (2/4, 50%); paraolfactory sulcus at 29 ± 2 weeks (2/4, 50%); inferior frontal sulcus at 30 ± 3 weeks (2/4, 50%); transverse occipital sulcus at 30 ± 3 weeks (2/4, 50%); occipitotemporal sulcus at 30 ± 3 weeks (2/4, 50%); marginal branch of the cingulate sulcus at 30 ± 3 weeks (2/4, 50%); paracentral sulcus at 30 ± 3 weeks (2/4, 50%); subparietal sulcus at 30 ± 3 weeks (2/4, 50%); inferior temporal sulcus at 31 ± 3 weeks (3/6, 50%); transverse temporal sulcus at 33 ± 3 weeks (6/8, 75%); and secondary sulcus at 38 ± 3 weeks (2/4, 50%). Conclusions The brain is subjected to considerable morphological changes throughout gestation. During fetal brain development the cortex begins to fold in, thereby increasing the cortical surface. All primary sulci are formed during fetal life. The appearance of each sulcus follows a characteristic timing pattern, which may be used as one of the reliable guides pertinent to gestational age and normal fetal development.


2021 ◽  
Author(s):  
◽  
Monica P. Strawn

Two experiments were conducted to investigate molecular regulation that impacts fetal brain development in pigs. In the first experiment (Chapter 2), gene expression was profiled by RNA sequencing (RNA-seq) to examine the whole transcriptome of the male (M) and female (F) fetal brain at gestation day (d) 45, 60 and 90. The analysis showed fewer differentially expressed genes (DEGs) in the brain of male and female fetuses in earlier gestation (d45-d60) when compared to late gestation (d60-d90). The homeobox (HOX) A5 gene that regulates pattern formation in early development was in the top upregulated DEGs between d45 to d60 in fetuses of both sexes. This study also found HOX B5 and D3 genes were in the top upregulated genes between d45 and d60 of the fetal brain of females, but not males. The second experiment (Chapter 3) investigated DNA methylation in pigs. DNA methylation in the fetal brain of both sexes at the same three gestation days was performed by enzymatic methyl sequencing (EM-seq). Hotspots of methylation in specific chromosomal regions were observed in the analysis. The analysis identified 1,475 sites in the pig genome that were methylated in the fetal brain, irrespective of sex, during development. The same sites were methylated in a canonically correlated manner in the blood of the adult stage, both in sows and boars. This is consistent with the Dilman theory of developmental aging (DevAge), which suggests that aging and early development of the brain are regulated by common molecular processes. A comparative analysis (Chapter 4) compared the gene expression patterns in the fetal brain and placenta between pigs and mice. The analysis identified 112 genes that were expressed (mean FPKM > 10) in the fetal brain of both species but not expressed (mean FPKM < 1) in the placenta of either species, and 10 genes that were expressed in the placenta of both species but not expressed in the fetal brain. In-silico analysis of the transcription factor binding sites in the 500 bp of the upstream DNA of these common genes revealed that they were commonly regulated by the RE1 silencing transcription factor (REST), which is a multifaceted transcription factor that acts as a master regulator of neurogenesis as well as controls neural excitation and the aging processes.


PEDIATRICS ◽  
1991 ◽  
Vol 88 (5) ◽  
pp. 1059-1062
Author(s):  
KARIN B. NELSON

"Consider what must be accomplished during the course of fetal brain development. In effect, in a few months the entire work of hundreds of millions of years of evolution must be reachieved. . . . Tens of billions of neurons must be born. . . . These new cells must find their way to their anatomical destinations, sometimes moving over substantial distances in an embryo that is constantly changing in form. . . Once the cell is fixed in place, the axon must find its way to its own destination. . . . They must not only get where they are going and make a connection, but they must avoid making any number of other connections that they might wrongly make in places they pass. Each nerve cell must develop one or more of at least a dozen neurotransmitters. . . ." The product of that miracle is the most complicated object in the known universe, a human brain. In this "Decade of the Brain," we can anticipate the emergence of a great deal more information about how the nervous system develops, prenatally and thereafter, and how and when that development can go awry. That information will come from laboratories, clinics, and nurseries. Neuroimaging of the infant brain, a subject now producing a rich harvest in journals of pediatrics, neurology, radiology, and obstetrics, will contribute important new information about the processes of brain development in our species, the timing of derailment from the normal course of brain development, and some aspects of pathogenesis. Neuropathology and the enormous flowering of new approaches in the basic and clinical neurosciences will help in explication of the mechanisms of maldevelopment and early injury. And we can hope that identification of mechanisms will allow us to develop strategies to prevent at least some of the problems leading to prenatal damage of the developing human brain.


2020 ◽  
Author(s):  
Colleen P.E. Rollins ◽  
Jane R. Garrison ◽  
Maite Arribas ◽  
Aida Seyedsalehi ◽  
Zhi Li ◽  
...  

Background: All perception is a construction of the brain from sensory input. Our first perceptions begin during gestation, making fetal brain development fundamental to how we experience a diverse world. Hallucinations are percepts without origin in physical reality that occur in health and disease. Despite longstanding research on the brain structures supporting hallucinations and on perinatal contributions to the pathophysiology of schizophrenia, what links these two distinct lines of research remains unclear. Methods: We studied two independent datasets of patients with schizophrenia who underwent clinical assessment and 3T structural magnetic resonance (MR) imaging from the United Kingdom and Shanghai, China (n = 181 combined) and 63 healthy controls from Shanghai. Participants were stratified into those with (n = 79 UK; n = 22 Shanghai) and without (n = 43 UK; n = 37 Shanghai) hallucinations from the PANSS P3 scores for hallucinatory behaviour. We quantified the length, depth, and asymmetry indices of the paracingulate and superior temporal sulci (PCS, STS) from MR images and constructed cortical folding covariance matrices organized by large-scale networks. Results: In both ethnic groups, we replicated a significantly shorter left PCS in patients with hallucinations compared to those without, and healthy controls. Reduced PCS length and STS depth corresponded to focal deviations in their geometry and to significantly increased covariance within and between areas of the salience and auditory networks. Conclusion: The discovery of neurodevelopmental alterations contributing to hallucinations establishes testable models for these enigmatic, sometimes highly distressing, perceptions and provides mechanistic insight into the pathological consequences of prenatal origins.


Author(s):  
Fereshteh Motamedi ◽  
◽  
Fariba Khodagholi ◽  
Leila Dargahi ◽  
Hamid Gholami Pourbadie ◽  
...  

Peroxisomes are the essential organelles in lipid metabolism. They contain enzymes for β-oxidation of very-long-chain fatty acids, which cannot break down in mitochondria. A reduced expression in hepatic Acyl-CoA oxidase1 (ACOX1), a peroxisome β-oxidation enzyme, followed by modification of the brain fatty acid profile has been seen in aged rodents. These studies have suggested a potential role for peroxisome β-oxidation in brain aging. This study was designed to examine the effect of hepatic ACOX1 inhibition on brain fatty acid composition and neuronal cell activities of young rats (200-250 g). A specific ACOX1 inhibitor, 10, 12- tricosadiynoic acid (TDYA), 100 μg/kg (in olive oil) was given by daily gavage administration for 25 days in male Wistar rats. The brain fatty acid composition and electrophysiological properties of dentate gyrus granule cells were determined by gas chromatography and whole-cell patch-clamp, respectively. A significant increase in C20, C22, C18:1, C20:1, and a decrease of C18, C24, C20:3n6 and C22:6n3 were found in TDYA treated rats compared to the control group. The results show that ACOX1 inhibition changes fatty acid composition similar to old rats. ACOX1 inhibition caused hyperpolarization of resting membrane potential, and also reduction of input resistance, action potential duration, and spike firing. Moreover, ACOX1 inhibition increased rheobase current and afterhyperpolarization amplitude in granule cells. The results indicate, systemic inhibition of ACOX1 causes hypo-excitability of neuronal cells. These findings provide a new evidence on the involvement of peroxisome function and hepatic ACOX1 activity in brain fatty acid profile and the electrophysiological properties of dentate gyrus cells.


2003 ◽  
Vol 76 (2) ◽  
pp. 187-195 ◽  
Author(s):  
Brian K. Speake ◽  
Frederic Decrock ◽  
Peter F. Surai ◽  
Nicholas A. R. Wood ◽  
René Groscolas

2020 ◽  
Vol 128 (06/07) ◽  
pp. 414-422
Author(s):  
Heiko Krude ◽  
Heike Biebermann ◽  
Markus Schuelke ◽  
Timo D. Müller ◽  
Matthias Tschöp

AbstractDespite its first description more than 75 years ago, effective treatment for “Allan-Herndon-Dudley-Syndrome (AHDS)”, an X-linked thyroid hormone transporter defect, is unavailable. Mutations in the SLC16A2 gene have been discovered to be causative for AHDS in 2004, but a comprehensive understanding of the function of the encoded protein, monocarboxylate transporter 8 (MCT8), is incomplete. Patients with AHDS suffer from neurodevelopmental delay, as well as extrapyramidal (dystonia, chorea, athetosis), pyramidal (spasticity), and cerebellar symptoms (ataxia). This suggests an affection of the pyramidal tracts, basal ganglia, and cerebellum, most likely already during fetal brain development. The function of other brain areas relevant for mood, behavior, and vigilance seems to be intact. An optimal treatment strategy should thus aim to deliver T3 to these relevant structures at the correct time points during development. A potential therapeutic strategy meeting these needs might be the delivery of T3 via a “Trojan horse mechanism” by which T3 is delivered into target cells by a thyroid hormone transporter independent T3 internalization.


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