scholarly journals Atlantic salmon (Salmo salar) require increased dietary levels of B-vitamins when fed diets with high inclusion of plant based ingredients

PeerJ ◽  
2016 ◽  
Vol 4 ◽  
pp. e2493 ◽  
Author(s):  
Gro-Ingunn Hemre ◽  
Erik-Jan Lock ◽  
Pål Asgeir Olsvik ◽  
Kristin Hamre ◽  
Marit Espe ◽  
...  

Aiming to re-evaluate current recommendations for nutrient supplementations when Atlantic salmon are fed diets based on plant ingredients, two regression experiments, with parr and post-smolt, were conducted. A control diet was included to evaluate if ingredients supplied sufficient nutrients without any added nutrient package (NP). The nutrient package consisted of vitamins B, C, E, minerals, cholesterol, methionine, taurine and histidine. This paper focus on B-vitamins. In parr, growth, health and welfare parameters responded on NP additions, but this was not observed in the seawater stage. During three months of feeding, parr tripled their weight. Parr given diets added the NP above NRC (2011) showed improved protein retention, and reduced liver and viscera indices. Post-smolt fed the same diets during five months showed a doubling of weight, but did not respond to the variation in NP to the same extent as parr. Significant regressions were obtained in body compartments for several of the B-vitamins in the premix. Whole body biotin concentration was unaffected by micronutrient premix level, and mRNA expression of the enzymes dependent of biotin showed only weak increases with increased biotin. Muscle thiamine plateaued at a diet level similar to NRC (2011) recommendation in freshwater, and showed stable values independent on premix addition in seawater. The mRNA expression of the enzyme G6PDH (glucose-6-phosphate dehydrogenase) is sensitive to thiamine availability; results did not indicate any need to add thiamine above levels recommended for fish in general. Niacin showed a steady increase in whole body concentrations as feed niacin increased. Muscle riboflavin peaked at a diet level of 12.4 mg kg−1. Sufficient riboflavin is important to avoid e.g., development of cataract. Cataract was not registered to be any problem, neither in fresh- nor in seawater. Cobalamin (B12) in muscle and liver was saturated at 0.17 mg kg−1diet. Muscle pyridoxine showed a dose-dependent level in muscle, and peaked around 10 mg kg−1diet. White muscle ASAT (asparagine amino transferase) activity steadily increased, with indications of stable values when dietary pyridoxine was around 10–16 mg kg−1diet. Pantothenic acid increased in gill tissue up to a level of 5.5 mg kg−1soft gill tissue; at a dietary level of 22 mg kg−1. Improved performance, and coverage of metabolic need for niacin was at a dietary level of 66 mg kg−1, riboflavin 10–12 mg kg−1, pyridoxine 10 mg kg−1and panthotenic acid 22 mg kg−1. Based on these results, recommended B-vitamin supplementation in plant based diets for Atlantic salmon should be adjusted.

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e12028
Author(s):  
Chandrasekar Selvam ◽  
Mark D. Powell ◽  
Nina S. Liland ◽  
Grethe Rosenlund ◽  
Nini H. Sissener

The aim of the study was to investigate the influence of dietary level and ratio of n-6/n-3 fatty acids (FA) on growth, disease progression and expression of immune and inflammatory markers in Atlantic salmon (Salmo salar) following challenge with Paramoeba perurans. Fish (80 g) were fed four different diets with different ratios of n-6/n-3 FA; at 1.3, 2.4 and 6.0 and one diet with ratio of 1.3 combined with a higher level of n-3 FA and n-6 FA. The diet with the n-6/n-3 FA ratio of 6.0 was included to ensure potential n-6 FA effects were revealed, while the three other diets were more commercially relevant n-6/n-3 FA ratios and levels. After a pre-feeding period of 3 months, fish from each diet regime were challenged with a standardized laboratory challenge using a clonal culture of P. perurans at the concentration of 1,000 cells L−1. The subsequent development of the disease was monitored (by gross gill score), and sampling conducted before challenge and at weekly sampling points for 5 weeks post-challenge. Challenge with P. perurans did not have a significant impact on the growth of the fish during the challenge period, but fish given the feed with the highest n-6/n-3 FA ratio had reduced growth compared to the other groups. Total gill score for all surfaces showed a significant increase with time, reaching a maximum at 21 days post-challenge and declined thereafter, irrespective of diet groups. Challenge with P. perurans influenced the mRNA expression of examined genes involved in immune and inflammatory response (TNF-α, iNOS, IL4-13b, GATA-3, IL-1β, p53, COX2 and PGE2-EP4), but diet did not influence the gene expression. In conclusion, an increase in dietary n-6/n-3 FA ratio influenced the growth of Atlantic salmon challenged with P. perurans; however, it did not alter the mRNA expression of immune genes or progression of the disease.


2011 ◽  
Vol 106 (5) ◽  
pp. 633-647 ◽  
Author(s):  
Bente E. Torstensen ◽  
Marit Espe ◽  
Ingunn Stubhaug ◽  
Øyvind Lie

In order to study whether lipid metabolism may be affected by maximum replacement of dietary fish oil and fish meal with vegetable oils (VO) and plant proteins (PP), Atlantic salmon (Salmo salarL.) smolts were fed a control diet containing fish oil and fish meal or one of three plant-based diets through the seawater production phase for 12 months. Diets were formulated to meet all known nutrient requirements. The whole-body lipid storage pattern was measured after 12 months, as well as post-absorptive plasma, VLDL and liver TAG. To further understand the effects on lipid metabolism, expression of genes encoding for proteins involved in VLDL assembly (apoB100), fatty acid uptake (FATP1, cd36, LPL and FABP3, FABP10 and FABP11) were measured in liver and visceral adipose tissue. Maximum dietary VO and PP increased visceral lipid stores, liver TAG, and plasma VLDL and TAG concentrations. Increased plasma TAG correlated with an increased expression of apoB100, indicating increased VLDL assembly in the liver of fish fed the high-plant protein- and VO-based diet. Atlantic salmon fed intermediate replacement levels of VO or PP did not have increased body fat or visceral mass. Overall, the present results demonstrate an interaction between dietary lipids and protein on lipid metabolism, increasing overall adiposity and TAG in the body when fish meal and fish oil are replaced concomitantly at maximised levels of VO and PP.


Endocrinology ◽  
2016 ◽  
Vol 157 (12) ◽  
pp. 4943-4960 ◽  
Author(s):  
Sandip K. Bose ◽  
Irina Hutson ◽  
Charles A. Harris

Exogenous glucocorticoid administration results in hyperglycemia, insulin resistance, hepatic dyslipidemia, and hypertension, a constellation of findings known as Cushing’s syndrome. These effects are mediated by the glucocorticoid receptor (GR). Because GR activation in liver and adipose has been implicated in metabolic syndrome (MS), we wanted to determine the role of GR in these tissues in the development of MS. Because GR knockout (KO) mice (whole-body KO) exhibit perinatal lethality due to respiratory failure, we generated tissue-specific (liver or adipose) GRKO mice using cre-lox technology. Real-time PCR analysis of liver mRNA from dexamethasone-treated wildtype (WT) and liver GRKO mice indicated that hepatic GR regulates the expression of key genes involved in gluconeogenesis and glycogen metabolism. Interestingly, we have observed that liver-specific deletion of GR resulted in a significant increase in mRNA expression of key genes involved in gluconeogenesis and glycogen metabolism in kidney tissue, indicating a compensatory mechanism to maintain glucose homeostasis. We have also observed that GR plays an important role in regulating the mRNA expression of key genes involved in lipid metabolism. Liver GRKO mice demonstrated decreased fat mass and liver glycogen content compared with WT mice administered dexamethasone for 2 weeks. Adipose-specific deletion of GR did not alter glucose tolerance or insulin sensitivity of adipose GRKO mice compared with WT mice administrated dexamethasone. This indicates that liver GR might be more important in development of MS in dexamethasone-treated mice, whereas adipose GR plays a little role in these paradigms.


Author(s):  
Paul J. Rozance ◽  
Stephanie R Wesolowski ◽  
Sonnet S. Jonker ◽  
Laura D Brown

Fetal skeletal muscle growth requires myoblast proliferation, differentiation, and fusion into myofibers in addition to protein accretion for fiber hypertrophy. Oxygen is an important regulator of this process. Therefore, we hypothesized that fetal anemic hypoxemia would inhibit skeletal muscle growth. Studies were performed in late gestation fetal sheep that were bled to anemic, and therefore hypoxemic, conditions beginning at ~125 days of gestation (term = 148 days) for 9 ± 0 days (n=19) and compared to control fetuses (n=16). A metabolic study was performed on gestational day ~134 to measure fetal protein kinetic rates. Myoblast proliferation and myofiber area were determined in biceps femoris (BF), tibialis anterior (TA), and flexor digitorum superficialis (FDS) muscles. mRNA expression of muscle regulatory factors was determined in BF. Fetal arterial hematocrit and oxygen content were 28% and 52% lower, respectively, in anemic fetuses. Fetal weight and whole-body protein synthesis, breakdown, and accretion rates were not different between groups. Hindlimb length, however, was 7% shorter in anemic fetuses. TA and FDS muscles weighed less and FDS myofiber area was smaller in anemic fetuses compared to controls. The percentage of Pax7+ myoblasts that expressed Ki67 was lower in BF and tended to be lower in FDS from anemic fetuses indicating reduced myoblast proliferation. There was less MYOD and MYF6 mRNA expression in anemic vs. control BF consistent with reduced myoblast differentiation. These results indicate that fetal anemic hypoxemia reduced muscle growth. We speculate that fetal muscle growth may be improved by strategies that increase oxygen availability.


2021 ◽  
Author(s):  
Shang-Wu Shih ◽  
Jia-Jiun Yan ◽  
Yi-Hsing Wang ◽  
Yi-Ling Tsou ◽  
Ling Chiu ◽  
...  

Estrogen-related receptors (ERRs) are known to function in mammalian kidney as key regulators of ion transport-related genes; however, a comprehensive understanding of the physiological functions of ERRs in vertebrate body fluid ionic homeostasis is still elusive. Here, we used medaka (Oryzias melastigma), a euryhaline teleost, to investigate how ERRs are involved in ion regulation. After transferring medaka from hypertonic seawater to hypotonic freshwater (FW), the mRNA expression levels of errγ2 were highly upregulated, suggesting that ERRγ2 may play a crucial role in ion uptake. In situ hybridization and immunofluorescence staining showed that errγ2 was specifically expressed in ionocytes, the cells responsible for Na+/Cl- transport. In normal FW, ERRγ2 morpholino knockdown caused reductions in the mRNA expression of Na+/Cl- cotransporter (NCC), the number of NCC ionocytes, Na+/Cl- influxes of ionocytes, and whole-body Na+/Cl- contents. In FW with low Na+ and low Cl-, the expression levels of mRNA for Na+/H+ exchanger 3 (NHE3) and NCC were both decreased in ERRγ2 morphants. Treating embryos with DY131, an agonist of ERRγ, increased the whole-body Na+/Cl- contents and ncc mRNA expression in ERRγ2 morphants. As such, medaka ERRγ2 may control Na+/Cl- uptake by regulating ncc and/or nhe3 mRNA expression and ionocyte number, and these regulatory actions may be subtly adjusted depending on internal and external ion concentrations. These findings not only provide new insights into the underpinning mechanism of actions of ERRs, but also enhance our understanding of their roles in body fluid ionic homeostasis for adaptation to changing environments during vertebrate evolution.


2006 ◽  
Vol 26 (1) ◽  
pp. 15-34 ◽  
Author(s):  
Richard N. Morrison ◽  
Glenn A. Cooper ◽  
Ben F. Koop ◽  
Matthew L. Rise ◽  
Andrew R. Bridle ◽  
...  

Neoparamoeba spp. are amphizoic amoebae with the capacity to colonize the gills of some marine fish, causing AGD. Here, the gill tissue transcriptome response of Atlantic salmon ( Salmo salar L.) to AGD is described. Tanks housing Atlantic salmon were inoculated with Neoparamoeba spp. and fish sampled at time points up to 8 days postinoculation (pi.). Gill tissues were taken from AGD-affected fish, and a DNA microarray was used to compare global gene expression against tissues from AGD-unaffected fish. A total of 206 genes, representing 190 unique transcripts, were reproducibly identified as up- or downregulated in response to Neoparamoeba spp. infection. Informative transcripts having GO biological process identifiers were grouped according to function. Although a number of genes were placed into each category, no distinct patterns were observed. One Atlantic salmon cDNA that was upregulated in infected gill relative to noninfected gill at 114 and 189 h pi. showed significant identity with the Xenopus, mouse, and human anterior gradient-2 (AG-2) homologs. Two Atlantic salmon AG-2 mRNA transcripts, designated asAG-2/1 and asAG-2/2, were cloned, sequenced, and shown to be predominantly expressed in the gill, intestine, and brain of a healthy fish. In AGD-affected fish, differential asAG-2 expression was confirmed in samples used for microarray analyses as well as in AGD-affected gill tissue taken from fish in an independent experiment. The asAG-2 upregulation was restricted to AGD lesions relative to unaffected tissue from the same gill arch, while p53 tumor suppressor protein mRNA was concurrently downregulated in AGD lesions. Differential expression of p53-regulated transcripts, proliferating cell nuclear antigen and growth arrest and DNA damage-inducible gene-45β (GADD45β) in AGD lesions, suggests a role for p53 in AGD pathogenesis. Thus AGD may represent a novel model for comparative analysis of p53 and p53-regulated pathways.


2016 ◽  
Vol 7 (2) ◽  
pp. 26
Author(s):  
Wanmi Nathaniel ◽  
Onyeanusi I. Barth ◽  
Nzalak J. Oliver ◽  
Aluwong Tanang

<p class="jbls-body"><span lang="EN-GB">A total of one hundred and seventy-three fertilized eggs were used for morphometry, gross and histological studies. At day 4 of incubation, the mean body weight of the helmeted guinea fowl embryo was 0.6401 ± 0.0211 g. It was at day 10 of incubation that there was an increase in the whole body weight of the embryo to be 0.8650 ± 0.676 g. The whole brain weight indicated relative increased at day 4 as compared to that of the whole body weight. Graphically, there were steady increase in the body, brain and optic lobe weights. Histologically, cells and neurones that make up the optic lobe is probably as a result of the migration of immature cells from the ventricular neuroepithelium. </span></p>


2010 ◽  
Vol 298 (5) ◽  
pp. E920-E929 ◽  
Author(s):  
Esben S. Buhl ◽  
Thomas Korgaard Jensen ◽  
Niels Jessen ◽  
Betina Elfving ◽  
Christian S. Buhl ◽  
...  

Low birth weight (LBW) is associated with type 2 diabetes and depression, which may be related to prenatal stress and insulin resistance as a result of chronic hypothalamic-pituitary-adrenal (HPA) axis hyperactivity. We examined whether treatment with a selective serotonin reuptake inhibitor [escitalopram (ESC)] could downregulate HPA axis activity and restore insulin sensitivity in LBW rats. After 4–5 wk of treatment, ESC-exposed LBW (SSRI-LBW) and saline-treated control and LBW rats (Cx and LBW) underwent an oral glucose tolerance test or a hyperinsulinemic euglycemic clamp to assess whole body insulin sensitivity. Hepatic phospho enolpyruvate carboxykinase (PEPCK) mRNA expression and red skeletal muscle PKB Ser473phosphorylation were used to assess tissue-specific insulin sensitivity. mRNA expression of the hypothalamic mineralocorticoid receptor was fivefold upregulated in LBW ( P < 0.05 vs. Cx), accompanied by increased corticosterone release during restraint stress and total 24-h urinary excretion ( P < 0.05 vs. Cx), whole body insulin resistance ( P < 0.001 vs. Cx), and impaired insulin suppression of hepatic PEPCK mRNA expression ( P < 0.05 vs. Cx). Additionally, there was a tendency for reduced red muscle PKB Ser473phosphorylation. The ESC treatment normalized corticosterone secretion ( P < 0.05 vs. LBW), whole body insulin sensitivity ( P < 0.01) as well as postprandial suppression of hepatic mRNA PEPCK expression ( P < 0.05), and red muscle PKB Ser473phosphorylation ( P < 0.01 vs. LBW). We conclude that these data suggest that the insulin resistance and chronic HPA axis hyperactivity in LBW rats can be reversed by treatment with an ESC, which downregulates HPA axis activity, lowers glucocorticoid exposure, and restores insulin sensitivity in LBW rats.


2019 ◽  
Vol 149 (2) ◽  
pp. 270-279 ◽  
Author(s):  
Dalila Azzout-Marniche ◽  
Catherine Chaumontet ◽  
Julien Piedcoq ◽  
Nadezda Khodorova ◽  
Gilles Fromentin ◽  
...  

ABSTRACT Background We have reported large differences in adiposity (fat mass/body weight) gain between rats fed a low-fat, high-starch diet, leading to their classification into carbohydrate “sensitive” and “resistant” rats. In sensitive animals, fat accumulates in visceral adipose tissues, leading to the suggestion that this form of obesity could be responsible for rapid development of metabolic syndrome. Objective We investigated whether increased amylase secretion by the pancreas and accelerated starch degradation in the intestine could be responsible for this phenotype. Method Thirty-two male Wistar rats (7-wk-old) were fed a purified low-fat (10%), high-carbohydrate diet for 6 wk, in which most of the carbohydrate (64% by energy) was provided as corn starch. Meal tolerance tests of the Starch diet were performed to measure glucose and insulin responses to meal ingestion. Indirect calorimetry combined with use of 13C-labelled dietary starch was used to assess meal-induced changes in whole body and starch-derived glucose oxidation. Real-time polymerase chain reaction was used to assess mRNA expression in pancreas, liver, white and brown adipose tissues, and intestine. Amylase activity was measured in the duodenum, jejunum, and ileum contents. ANOVA and regression analyses were used for statistical comparisons. Results “Resistant” and “sensitive” rats were separated according to adiposity gain during the study (1.73% ± 0.20% compared with 4.35% ± 0.36%). Breath recovery of 13CO2 from 13C-labelled dietary starch was higher in “sensitive” rats, indicating a larger increase in whole body glucose oxidation and, conversely, a larger decrease in lipid oxidation. Amylase mRNA expression in pancreas, and amylase activity in jejunum, were also higher in sensitive rats. Conclusion Differences in digestion of starch can promote visceral fat accumulation in rats when fed a low-fat, high-starch diet. This mechanism may have important implications in human obesity.


2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Lauren Woodie ◽  
Robert Johnson ◽  
Bulbul Ahmed ◽  
Michael Greene

Abstract Objectives Mammalian circadian rhythms are dictated by solar signals transmitted to the hypothalamic suprachaismatic nucleus (SCN). Although the SCN is the central clock for circadian rhythms, molecular clocks are found in every cell and are composed of the core clock proteins BMAL1, CLOCK/NPAS2, Period (Per) and Cryptochrome (Cry). Disruptions in the core clock occur in peripheral tissues after Western diet (WD) feeding and contribute to WD-induced metabolic disease. The mammalian center of memory, the hippocampus, is also sensitive to WD-induced dysfunction, but whether the WD disrupts the hippocampal core clock is not known. The present research explores this gap in our knowledge by examining hippocampal core clock rhythmicity in a mouse model of WD-induced obesity. Methods Mice were maintained on either standard rodent chow with tap water or a 45%/kcal fat WD with a 4% sugar solution (WD + S). Diurnal metabolic rhythms were collected for 24 h in metabolic cages during the 16th week of diet exposure. Livers, hypothalami and hippocampi were then collected at 4-h increments over 24 h. mRNA expression was measured using RT-qPCR and assessed by cosinor-based rhythmometry. Results WD + S feeding significantly increased body weight and normalized liver weight (P < 0.001) and significantly dampened diurnal rhythms of whole-body metabolism (P < 0.05). As expected, the WD + S also induced significant alterations in the hepatic rhythmicity of bmal1 and cry1 expression (P < 0.05). In line with previous findings, the rhythm of the hypothalamic core clock did not significantly differ between the dietary groups. The hippocampal core clock, however, was significantly disrupted by the WD + S. Bmal1 and npas2 expression were phase shifted by 16 and 4 h, respectively, while per2 expression was significantly amplified across all measured time points in the WD + S group (P < 0.01). Conclusions WD + S feeding significantly alters the rhythmicity of core clock mRNA expression in the hippocampus. These results indicate that diet-induced disruptions of the core clock may have implications in memory diseases with significant circadian etiologies, such as Alzheimer's disease. Funding Sources Funding was provided by the Alabama Agricultural Experiment Station and the Auburn University Center for Neuroscience Initiative.


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