Dietary Krill Oil Research Articles

New Insights on the Effects of Krill Oil Supplementation, a High-Fat Diet, and Aging on Hippocampal-Dependent Memory, Neuroinflammation, Synaptic Density, and Neurogenesis.

Krill oil (KO) has been described as having the potential to ameliorate the detrimental consequences of a high-fat diet (HFD) on the aging brain, though the magnitude and mechanism of this benefit is unclear. We thus hypothesized that dietary KO supplementation could counteract the effects of cognitive aging and an HFD on spatial learning, neuroinflammation, neurogenesis, and synaptic density in the cortex and hippocampus of aged rats. Sixteen-month-old Sprague Dawley rats were fed for 12 weeks while being divided into four groups: control (CON); control with KO supplementation (CONKO); high-fat diet (HF); and high-fat diet with KO supplementation (HFKO). We measured food consumption, body mass, spatial memory (Morris water maze), microglia, neurogenesis, cytokine concentrations, and synaptic markers (post-synaptic density-95 and synaptophysin). Predictably, an HFD did induce significant differences in body weights, with the high-fat groups gaining more weight than the low-fat controls. However, KO supplementation did not produce significant changes in the other quantified parameters. Our results demonstrate that the dietary KO dose provided in the current study does not benefit hippocampal or cortical functions in an aging model. Our results provide a benchmark for future dosing protocols that may eventually prove to be beneficial.

Effect of dietary krill oil levels on the regulation of ovary development in Pacific white shrimp (Litopenaeus vannamei) broodstock

Krill oil is rich in phospholipids and has been proven to significantly promote ovarian development in shrimp. However, the optimal level and related mechanism are unknown. In this study, four isonitrogenous and isolipidic diets were prepared. These diets included different gradients of krill oil supplementation (3%, 6%, and 9%), with no-krill oil serving as a control. Female Litopenaeus vannamei broodstock with stage I ovarian development were fed these diets for 28 days. The results showed that the inclusion of krill oil in the diet had a positive effect on ovarian development in female shrimp, particularly at the 6% supplementation level. This was evident from the significant improvements in the gonadosomatic index and in the 17β-estradiol, progesterone, and methyl farnesoid levels. Moreover, 6% krill oil supplementation facilitated lipid accumulation in the hepatopancreas, promoted the deposition of yolk granules within the oocyte, and significantly enhanced the mobilization efficiency of triglycerides and total cholesterol from the hepatopancreas to the ovary. The upregulation of the serum metabolites choline and phosphorylcholine promotes the synthesis of phosphatidylcholine and triglycerides. Additionally, prostaglandin E2 stimulates the production of ovarian steroid hormones. Acamprosate influences the activity of glutamic acid, potentially leading to a reduction in the secretion of gonadal inhibitory hormones. Multiomics analysis revealed joint enrichment of differentially altered metabolites and differentially expressed genes in pathways involved in arachidonic acid metabolism, cholesterol metabolism, and ovarian steroid synthesis. Additionally, there was significant enrichment in glycerophospholipid metabolism. The expression of the cytosolic phospholipase A2 gene was upregulated in both the lipid metabolism and steroid synthesis pathways. Moreover, the mRNA expression levels of 3β-hydroxysteroid dehydrogenase/delta 5- > 4-isomeras, cytochrome P450 2 L1, and prostaglandin H synthase 2 were also upregulated in the ovarian steroid synthesis pathway. In conclusion, supplementing the diet with 6% krill oil is optimal for promoting lipid metabolism and steroid hormone secretion in female L. vannamei broodstock, thereby enhancing ovarian development and maturation.

Krill oil showed a good application potential as the dietary lipid source on the growth, physiology, nutritional quality, and flavor of the edible meat of the oriental river prawns (Macrobrachium nipponense)

An 8-week feeding trial was conducted to evaluate the effects of dietary krill oil (KO), fish oil (FO) and soybean oil (SO) on growth, nutritional quality and flavor of the edible meat of the oriental river prawns (Macrobrachium nipponense). The results revealed that SO and KO diets promoted the growth performance (P < 0.05). The activity of alanine aminotransferase in hemolymph of the FO group was significantly lower than that in the SO group (P < 0.05). The contents of total cholesterol in hemolymph in the SO and FO groups were significantly lower than those in the KO group (P < 0.05). Superoxide dismutase activity and glutathione content in the hepatopancreas were the lowest in the SO group (P < 0.05). Lipoprtein lipase and trypsin activities of the hepatopancreas decreased significantly in the KO group (P < 0.05). Among the fatty acids in meat, the contents of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) increased significantly in M. nipponense after feeding on animal lipid sources (FO and KO) (P < 0.05). The contents of umami and bitter free amino acids in the SO and KO groups were significantly higher than those in the FO group (P < 0.05), and the contents of adenosine monophosphate and inosine monophosphate were highest in the KO group (P < 0.05). The contents of bitter nucleotides hypoxanthine and hypoxanthine ribonucleoside were lowest in the KO group (P < 0.05). In general, compared with FO, the use of KO and SO as lipid sources in feed promoted the growth of M. nipponense, and KO significantly improved the antioxidant index of the hepatopancreas. FO and KO increased the contents of EPA and DHA in the edible meat of M. nipponense, and KO further enhanced the contents of amino acids and nucleotides responsible for flavor in the meat.

Effect of dietary krill oil supplementation on horse red blood cell membrane fatty acid composition and blood parameters.

Supplementation with marine-derived n-3 long-chain polyunsaturated fatty acids (LC PUFAs), eicosapentaenoic acid (EPA, 20:5 n-3) and docosahexaenoic acid (DHA, 22:6 n-3) is linked to beneficial health effects in both humans and horses. Krill oil (KO), which is extracted from the Antarctic krill (Euphausia superba), is well documented as a safe and biologically available dietary supplement in humans and several animal species, but there is a lack of documentation regarding its effect as a dietary ingredient for horses. The objective of this study was to test whether KO as a dietary supplement had the ability to raise horse red blood cell (RBC) membrane EPA and DHA, expressed as the n-3 index. Five nonworking Norwegian cold-blooded trotter horse geldings (body weight [BW]: 567 ± 38 kg) were supplemented with KO (10 mL/100 kg BW) for 35 days in a longitudinal study. Blood samples were analysed for RBC membrane fatty acid (FA) profile, haematology and serum biochemistry every 7th day. KO was well accepted by all horses, and no adverse health effects were observed during the 35-day trial period. KO supplementation affected the RBC membrane FA profile by increasing the n-3 index from Day 0 to 35 (Day 0: 0.53% vs. Day 35: 4.05% of total RBC FAs). The observed increase in the sum of EPA and DHA (p < 0.001), total n-3 FAs (p < 0.001) and the reduction of n-6 FAs (p < 0.044) resulted in a lower n-6:n-3 ratio (p < 0.001) by Day 35 of KO supplementation. In conclusion, the RBC n-3 index was increased and the general n-6:n-3 ratio was decreased in horses receiving 35-day dietary KO supplementation.

Preventive and Therapeutic Effects of Krill Oil on Obesity and Obesity-Induced Metabolic Syndromes in High-Fat Diet-Fed Mice.

Obesity increases the risks of metabolic syndromes including nonalcoholic fatty liver disease (NAFLD), diabetic dyslipidemia, and chronic kidney disease. Dietary krill oil (KO) has shown antioxidant and anti-inflammatory properties, thereby being a therapeutic potential for obesity-induced metabolic syndromes. Thus, the effects of KO on lipid metabolic alteration were examined in a high-fat diet (HFD)-fed mice model. The HFD model (n = 10 per group) received an oral gavage with distilled water as a control, metformin at 250 mg/kg, and KO at 400, 200, and 100 mg/kg for 12 weeks. The HFD-induced weight gain and fat deposition were significantly reduced in the KO treatments compared with the control. Blood levels were lower in parameters for NAFLD (e.g., alanine aminotransferase, and triglyceride), type 2 diabetes (e.g., glucose and insulin), and renal dysfunction (e.g., blood urea nitrogen and creatinine) by the KO treatments. The KO inhibited lipid synthesis through the modification of gene expressions in the liver and adipose tissues and adipokine-mediated pathways. Furthermore, KO showed hepatic antioxidant activities and glucose lowering effects. Histopathological analyses revealed that the KO ameliorated the hepatic steatosis, pancreatic endocrine/exocrine alteration, adipose tissue hypertrophy, and renal steatosis. These analyses suggest that KO may be promising for inhibiting obesity and metabolic syndromes.

New Insight Into the Molting and Growth in Crustaceans: Regulation of Energy Homeostasis Through the Lipid Nutrition

Organisms can regulate mitochondrial metabolic adaptation, further ameliorate the energy homeostasis to control the ATP production for the energy expenditure during the growth process under different physiological and nutritional conditions. Based on this understanding, the objective of the present study was to investigate how different dietary n-3 PUFA (polyunsaturated fatty acid) lipid sources modify the mitochondrial metabolic adaptation, and further affect the energy homeostasis and the growth of swimming crab (Portunus trituberculatus). A total of 120 swimming crab juveniles with an average initial weight of 10.17 ± 0.12 g were fed one of three diets (4 replicates/treatment) containing either fish oil (control), krill oil or linseed oil as dietary lipid sources for 8 weeks, and the effects of dietary lipid sources on the growth and energy homeostasis via the regulation of mitochondrial metabolic adaptation were evaluated. The study revealed that, compared with linseed oil rich in 18:3n-3, fish oil and krill oil rich in 20:5n-3 and 22:6n-3 significantly promoted the molting and growth of juvenile swimming crab, increased the ATP level, mitochondrial membrane potential, NAD+ substrate level, NAD+/NADH ratio and the mitochondrial DNA copy number. Furthermore, crabs fed the diet supplemented with krill oil can up-regulate the expression levels of genes related to energy metabolism. In addition, dietary krill oil also specifically improved the ability for scavenging free radicals produced in the process of physiological metabolism, reduced the level of lipid peroxidation and the degree of DNA oxidative damage, and improved the health status of swimming crab. The present study revealed the adaptation of mitochondrial metabolism and the regulation of the energy homeostasis of swimming crab to different dietary n-3 PUFA lipid sources, and provided a new insight into the relationship between the growth as well as molting and the energy homeostasis, which provided a novel insight into the lipid nutrition and energy metabolism of crustacean species.

Impact of Krill Oil Supplementation on Neuroinflammation and Spatial Memory in Aged Rats

ObjectiveInvestigate the potential of dietary krill oil (KO), a marine‐based, long chain, omega‐3 (n‐3) polyunsaturated fatty acid (PUFA), to negate the deleterious effects of high fat diets and aging on neuroinflammation and spatial learning in a rat model.Background/HypothesisKO exhibits anti‐inflammatory properties comparable to other sources of n‐3 PUFA, but with several biochemical advantages. Phospholipid‐bound fatty acids in KO exhibit improved bioavailability when compared to triacylglyceride bound n‐3 PUFA such as fish oil. Moreover, KO contains astaxanthin, a powerful antioxidant that counters harmful oxidative stress in the brain, as well as choline which is an essential neurotransmitter precursor with neuroprotective properties. Hence, we hypothesized that KO supplementation would improve deficiencies in spatial learning and elevated neuroinflammatory protein levels induced by high fat diet and normal aging in rats.MethodsThirty‐two male, Sprague Dawley rats, aged 15 months were divided into four dietary groups consisting of varying amounts of saturated fats, with and without krill oil supplementation: Control (CON), Control with krill oil (CONKO), High fat (HF), High fat with krill oil (HFKO). HF and CON experimental diets consisted of 60% and 23% calories from saturated fats, respectively. Food intake and body weight were assessed weekly. After 12‐weeks of dietary supplementation, Morris Water Maze (MWM) testing was conducted to compare spatial learning abilities between groups. Moreover, inflammatory cytokine concentrations, including interleukin (IL)‐1β, IL‐4, IL‐6, IL‐10 and tumor necrosing factor‐α (TNF‐α), were analyzed using multiplex bead‐based protein assays.ResultsDespite evidence of learning by each group over the course of MWM testing, no significant difference between dietary groups in reaching the platform was identified. Furthermore, no statistically significant difference in inflammatory cytokines was identified. Total food consumption was significantly less in the HF group when compared to CON (p=.047) and CONKO (p=.030), whereas body weight was significantly higher in the HFKO group when compared to CON (p=.024) and CONKO (p=.030). Otherwise, no significant difference in food consumption or body weight was identified.ConclusionsKO supplementation did not significantly improve the effects of aging and high fat diet consumption on spatial memory or neuroinflammatory signaling proteins. Some evidence suggests that the unique properties of KO, a more novel source n‐3 PUFA, have the potential to decrease neuroinflammation and improve cognition. Indeed, considering an aging population, the proliferation of western‐style diets, and the associated increase in neurodegenerative diseases such as Alzheimer’s disease, there is a need for preventive interventions. Further investigations are still needed to weigh the potential benefits of n‐3 dietary supplementation, aging, obesity, and neurodegenerative disease.

The comparative anti-cancer effects of krill oil and oxaliplatin in an orthotopic mouse model of colorectal cancer

BackgroundOur in vitro studies demonstrated that krill oil (KO) has anti-cancer potential. This study aimed to compare the anti-cancer effects of KO with a commonly used chemotherapeutic drug, oxaliplatin and to identify the molecular mechanisms associated with KO supplementation in a mouse model of colorectal cancer (CRC).MethodsThirty-six male Balb/c mice were randomly divided into six groups. Five groups received standard chow diet supplemented with KO (150 g/kg)), corn oil (150 g/kg), KO combined with ½ dose of oxaliplatin (1.5 mg/kg body weight/3 times per week), corn oil combined with ½ dose of oxaliplatin (1.5 mg/kg body weight/3 times per week), or a full dose of oxaliplatin (3 mg/kg body weight/3 times per week). The control (sham) group received a standard chow diet. Treatments started three weeks before and continued for three weeks after orthotopic CRC induction. The number of metastases, tumour weight and volume were quantified ex-vivo. The expression of cytochrome c, cleaved caspase-9 and -3, DNA damage, PD-L1, PD-L2 and HSP-70 were determined.ResultsA significant reductions in the weight and volume of tumours were observed in mice treated with KO and KO plus a ½ dose of oxaliplatin compared to the sham group, similar to oxaliplatin-treated mice. KO, and KO plus ½ dose of oxaliplatin significantly increased the expression of cytochrome c, cleaved caspase-9 and -3, and DNA damage and decreased expression of PD-L1, PD-L2 and HSP-70 in tumour tissues compared to the sham group.ConclusionsThe in vivo anti-cancer effects of KO are comparable with oxaliplatin. Thus, dietary KO supplementation has a great potential as a therapeutic/adjunctive agent for CRC treatment.

Hepatopancreas transcriptome analysis reveals the molecular responses to different dietary n-3 PUFA lipid sources in the swimming crab Portunus trituberculatus

n-3 LC-PUFA is vital to crustaceans for the growth, molting and development, while the precise molecular mechanism underlying the regulation of n-3 LC-PUFA is poorly investigated. Herein, an 8-week nutritional trial and transcriptome analysis were used to investigate the impacts of dietary n-3 PUFA lipid sources including fish oil (FO), krill oil (KO) and linseed oil (LO) on the transcriptome characteristics in hepatopancreas of swimming crab (Portunus trituberculatus). Crabs fed KO diet had significantly higher percent weight gain (PWG) and molting ratio (MR) than those of crabs fed other diets. The transcriptome analysis reveled that a total of 6567 unigenes were annotated in KEGG database, of which the expression of 1126 significantly altered in the KO vs FO group, while the expression of 921 unigenes changed in the LO vs FO group. The differentially expressed genes (DEGs) in KO vs FO comparison group involved in fat digestion and absorption, ABC transporters, adipocytokine signaling pathway, protein digestion and absorption, glycolysis/gluconeogenesis and HIF-1 signaling pathway. While dietary LO significantly altered the expression levels of genes involved in carbohydrate digestion and absorption, mineral absorption, protein processing in endoplasmic reticulum, glycosphingolipid biosynthesis and insect hormone biosynthesis. In addition, dietary KO significantly up-regulated the expression levels of cyp18a1 (participates in the process of ecdysteroids biosynthesis and further controls the molting of crustaceans), tryp (trypsin-like serine proteinases, resists the pathogen invasion), pla2 (phospholipase A2, regulates different inflammatory processes), ABC transporter (ATP-binding cassette transporter, transports amino acids, lipids and proteins into and out of the cell), cpt1 (carnitine palmitoyltransferase I, the major rate-limiting enzyme of mitochondrial fatty acid β-oxidation) and slc2 (solute carrier 2, mediates bidirectional glucose transport). Meanwhile, dietary LO could significantly down-regulated the expression level of cyp315a1 compared to dietary FO. To sum up, swimming crab fed with dietary krill oil could not only enhance the transport of glucose, lipids, fatty acids and other substrates, but also up-regulate the expression levels of genes related to molting, immunity and energy metabolism to promote molting and growth of swimming crab. The present study revealed the molecular responses of crabs to different dietary n-3 PUFA lipid sources, and further provided important clues with respect to elucidating the molecular mechanisms underlying the regulation of EPA and DHA on the molting and growth of swimming crab.

Untargeted lipidomics reveals metabolic responses to different dietary n-3 PUFA in juvenile swimming crab (Portunus trituberculatus)

While tissue fatty acid compositions reflect that of the dietary lipid source, little information is available on how dietary oils modify lipid class and molecular species profiles in hepatopancreas of crustacean. Herein, an 8-week nutritional trial and untargeted lipidomic analysis were used to investigate the impacts of dietary n-3 PUFA lipid sources including fish oil, krill oil and linseed oil on the lipidomic characteristics of hepatopancreas of swimming crab (Portunus trituberculatus). Dietary krill oil significantly increased distribution of 20:5n-3 and 22:6n-3 at sn-2 in phosphatidylcholine and phosphatidylethanolamine compared to fish oil. Fish oil intake promoted the deposition of 20:5n-3 and 22:6n-3 at sn-1,2,3 in triglyceride compared to linseed oil, which significantly increased the specific accumulation of 18:3n-3 at sn-1,3 in triglyceride and sn-2 in phosphatidylcholine and phosphatidylethanolamine. The study revealed metabolic responses to different dietary n-3 PUFA in swimming crab, which provided novel insight into the lipid nutrition of crustacean.

Growth performance, antioxidant capacity, tissue fatty acid composition and lipid metabolism of juvenile green mud crab Scylla paramamosain in response to different dietary n-3 PUFA lipid sources

An six-week feeding trial was conducted to evaluate the effects of dietary n-3 polyunsaturated fatty acid (n-3 PUFA) lipid sources on growth performance, antioxidant capacity, tissue fatty acid profiles, and expression levels of genes involved in lipid metabolism of juvenile green mud crab (Scylla paramamosain) (initial weight 45.3 ± 0.07 g). Three isonitrogenous and isoenergetic experimental diets were formulated to contain fish oil (FO), krill oil (KO) and linseed oil (LO), respectively. The results indicated that crabs fed the KO diet had significantly higher percent weight gain (PWG), specific growth rate (SGR) and feed efficiency (FE) than those fed the LO diet, while no statistic differences were observed between KO and FO diets. Dietary FO could significantly increase the concentrations of malondialdehyde (MDA) and lipid hydroperoxide (LPO) in hemolymph and hepatopancreas compared to dietary KO and LO, similar results were found in the levels of hepatopancreas 8-hydroxy-2-deoxyguanosine (8-OHDG). Crabs fed the KO diet could significantly increase the activities of total superoxide dismutase (T-SOD) and catalase (CAT) in comparison with FO and LO diets. Crabs fed with FO and KO had significantly higher contents of 20:5n-3 (EPA) and 22:6n-3 (DHA) in hepatopancreas and muscle than those fed with LO. While dietary LO could significantly promote the accumulation of C18:3n-3 (ALA) in hepatopancreas and muscle. The anabolic pathway relevant genes: fas and 6 pg d were up-regulated in KO diet. The catabolic pathway relevant genes, hsl, was up-regulated in FO and KO diets, cpt1, was up-regulated in KO diet. Moreover, crabs fed diet supplemented with KO could significantly increase the expression levels of srb2, srebp1 and hnf4α. These findings will provide the reference for the development of the diet for the growth stage of S. paramamosain, and could contribute to deepen the understanding of the physiological metabolism of dietary fatty acids for S. paramamosain.

Lipase Treatment of Dietary Krill Oil, but Not Fish Oil, Enables Enrichment of Brain Eicosapentaenoic Acid and Docosahexaenoic Acid.

Currently available omega-3 fatty acid supplements do not enrich the docosahexaenoic acid (DHA) of the adult brain because they are absorbed as triacylglycerol, whereas the transporter at the blood brain barrier requires lysophosphatidylcholine (LPC)-DHA. The hypothesis that treatment of krill oil (KO), which contains DHA/eicosapentaenoic acid (EPA) at the SN2 position of phosphatidylcholine, with SN1-specific lipase will generate LPC-DHA/EPA and which can be absorbed intact and transported into the brain, is tested. KO and fish oil (FO) are treated with Mucor meihei lipase, incorporated into AIN 93G diet, and fed to 2-month-old mice for 30 days. Fatty acid composition is analyzed by gas chromatography/mass spectroscopy. Brain derived neurotrophic factor (BDNF) is measured by ELISA. Lipase-treated (LT) KO increases brain DHA and EPA, respectively, 5-and 70-fold better than untreated (UT) KO. FO, whether lipase-treated or not, has no effect on brain DHA/EPA. LTKO is also more efficient in enriching liver DHA/EPA, but less efficient than UTKO and FO in enriching adipose tissue and heart. Brain BDNF is significantly increased by LTKO, but only marginally by other preparations. Pretreatment of dietary KO with lipase enables it to efficiently increase brain DHA/EPA because of the generation of LPC-DHA/EPA.

Regulation of Dietary Lipid Sources on Tissue Lipid Classes and Mitochondrial Energy Metabolism of Juvenile Swimming Crab, Portunus trituberculatus.

An 8-weeks feeding trial with swimming crab, Portunus trituberculatus, was conducted to investigate the effects of different dietary lipid sources on the lipid classes, lipid metabolism, and mitochondrial energy metabolism relevant genes expression. Six isonitrogenous and isolipidic experimental diets were formulated to contain fish oil (FO), krill oil (KO), palm oil (PO), rapeseed oil (RO), soybean oil (SO), and linseed oil (LO), respectively. A total of 270 swimming crab juveniles (initial weight 5.43 ± 0.03 g) were randomly divided into six diets with three replications, each consisted of 45 juvenile crabs. The results revealed that crabs fed KO had highest lipid content in hepatopancreas and free fatty acids in serum among all diets. The anabolic pathway relevant genes: fas and acc were up-regulated in KO diet. The catabolic pathway relevant genes, hsl, was up-regulated in LO diet, while cpt1 was up-regulated in KO diet. Whereas, the genes involved in the transport and uptake of fatty acids such as fabp1 and fatp4 were down-regulated in crab fed PO and RO diets. Furthermore, the gene expression levels of transcription factors: srebp-1 and hnf4α in KO and SO diets were the highest among all diets. FO and KO diets had significantly higher unsaturation index of mitochondrial membrane than others. The genes related to mitochondrial energy metabolism, such as Atpase6, sirt1, and sirt3 were significantly up-regulated in KO and SO diets. In summary, dietary KO and SO supplementation could improve the lipid metabolism, promote energy production for juvenile swimming crab and improve physiological process and function including molting. These findings could contribute to deepen the understanding of the physiological metabolism of dietary fatty acids for swimming crab.

Accretion of Dietary Docosahexaenoic Acid in Mouse Tissues Did Not Differ between Its Purified Phospholipid and Triacylglycerol Forms.

Recent studies suggest that dietary krill oil leads to higher omega-3 polyunsaturated fatty acids (n-3 PUFA) tissue accretion compared to fish oil because the former is rich in n-3 PUFA esterified as phospholipids (PL), while n-3 PUFA in fish oil are primarily esterified as triacylglycerols (TAG). Tissue accretion of the same dietary concentrations of PL- and TAG-docosahexaenoic acid (22:6n-3) (DHA) has not been compared and was the focus of this study. Mice (n = 12/group) were fed either a control diet or one of six DHA (1%, 2%, or 4%) as PL-DHA or TAG-DHA diets for 4 weeks. Compared with the control, DHA concentration in liver, adipose tissue (AT), heart, and eye, but not brain, were significantly higher in mice consuming either PL- or TAG-DHA, but there was no difference in DHA concentration in all tissues between the PL- or TAG-DHA forms. Consumption of PL- and TAG-DHA at all concentrations significantly elevated eicosapentaenoic acid (20:5n-3) (EPA) in all tissues when compared with the control group, while docoshexapentaenoic acid (22:5n-6) (DPA) was significantly higher in all tissues except for the eye and heart. Both DHA forms lowered total omega-6 polyunsaturated fatty acids (n-6 PUFA) in all tissues and total monounsaturated fatty acids (MUFA) in the liver and AT; total saturated fatty acid (SFA) were lowered in the liver but elevated in the AT. An increase in the DHA dose, independent of DHA forms, significantly lowered n-6 PUFA and significantly elevated n-3 PUFA concentration in all tissues. Our results do not support the claim that the PL form of n-3 PUFA leads to higher n-3 PUFA tissue accretion than their TAG form.

Microbial diversity and composition in different gut locations of hyperlipidemic mice receiving krill oil.

Low-dose (LD, 100mgkg-1day-1), moderate-dose (MD, 200mgkg-1day-1), and high-dose (HD, 600mgkg-1day-1) krill oil treatments have a stepwise, enhanced effect on alleviating hyperlipidemia, and 16S rRNA sequencing of the fecal samples demonstrates that krill oil treatment alters microbial communities. Feces may not represent all microbial communities in the gastrointestinal (GI) tract. Therefore, in this study, the stored ileal and colon samples collected from LD and HD groups were sequenced, and the location-specific modulations of microbial communities were observed after krill oil treatments. The 16S rRNA sequencing of the ileal samples showed that the LD and HD groups have similar patterns between control and high-fat diet (HFD) treatments, and six most abundant genera and 40 operational taxonomic units that respond to krill oil treatment were identified. However, the 16S rRNA sequencing of the colon samples showed that LD krill oil shifts the structure from the HFD to that of the control, whereas the HD group was distributed between the control and HFD groups. The corresponding most abundant genera and responsive OTUs totaled 4 and 45, respectively. In conclusion, different gastrointestinal tract locations contain different microbial communities. These results will help to provide a comprehensive understanding of the role of dietary krill oil in modulating the gut microbiota and alleviating hyperlipidemia.

Dietary krill oil (Euphausia superba) alleviates oxidative stress and DNA damages bio-markers in an experimental model of cafeteria diet-induced insulin resistance in rats

Dietary krill oil (Euphausia superba) alleviates oxidative stress and DNA damages bio-markers in an experimental model of cafeteria diet-induced insulin resistance in rats

Dietary krill oil enhances neurocognitive functions and modulates proteomic changes in brain tissues of d-galactose induced aging mice.

The effects of dietary krill oil on neurocognitive functions and proteomic changes in brain tissues of d-galactose-induced aging mice were evaluated. Dietary krill oil enhanced the neurocognitive functions of aging mice with a significant (P < 0.05) decrease in escape latency and an increase in the number of times of crossing over the hidden platform during the Morris water maze test. Krill oil was also found to protect against oxidative damage, lipid peroxidation and neurodegenerative diseases. Oxidative stress biomarkers of aging mice administered with krill oil showed significant (P < 0.05) improvement with an increase in serum superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels; there were insignificant changes in the serum malondialdehyde (MDA) level. In terms of proteomic changes, krill oil resulted in upregulation of the Celsr3 and Ppp1r1b gene expression, which contribute to brain development, learning and memory behavior processes. In particular, the Ppp1r1b gene is associated with the inhibition of dopamine releases, which decreases the motivation for learning.

Effets thérapeutiques de la supplémentation en huile de krill (Euphausia superba) sur les marqueurs du stress oxydant et des dommages de l’ADN chez des rats soumis au régime cafétéria

AimTo evaluate the therapeutic effects of dietary krill oil supplementation in modulation of oxidative stress components and DNA oxidative damages marker in cafeteria diet-overfed-rats. Material and methodsEighteen aging male Wistar rats were divided into three groups of six each and were exposed for the ensuing 8 weeks to one of the diets: control group (TS) which was submitted to standard chow (330kcal/100g), containing 24% of proteins, 5% of lipids and 70% of carbohydrates. Cafeteria standard group (TC) exposed to cafeteria diet (420kcal/100g). The last group received a cafeteria diet enriched in oral force-feeding krill oil 2% (CK). The plasma and tissues pro-oxydant status were assessed by assaying thiobarbituric acid reactive substances, hydroperoxydes, and isoprostans. The determination of DNA oxidative damages was evaluated by the measurement of the major products of DNA oxidation (8-OHdG). ResultsExposure to a cafeteria diet increases the metabolic response to the radical attack and DNA oxidative damages in both plasma and key tissues involved in antioxidant defense. Krill oil supplementation in cafeteria diet relieves oxidative stress and DNA damages by lowering several lipid peroxidation components and the main marker of DNA oxidation in obese rats.

P2-12: Cell-based anti-oxydant activity of dietary krill oil enrichment in high fat-fed rats target tissues

Background Obesity has emerged as the biggest pandemic of our times growing parallel to type 2 diabetes. Its managment by several therapeutic approaches has been unable to completely inhibit different pathways involved the reactive oxygen species (ROS) production, lipid peroxidation and PKC activation. Coupled with recent evidences that highlight the role of ROS in the onset and progression of type 2 diabetes, the antioxidants have taken prime focus as potential pharmacological approach. Krill oil enriched in marine ω3 regulates numerous anti-inflammatory and antioxidative processes. The aim of our study was to determine whether enrichment with Krill oil (KO) protects insulin resistant target tissues of high fat-diet-fed rats against oxidative stress features. Methods The 6 – to 8-week-old mal Wistar rats weighing 160-200 g were randomly divided into three experimental groups consisting of 10 each and received one of the following three experimental diets during 8 weeks : standard laboratory chow (18kcal% fat, 58kcal% carbohydrates, 24kcal% proteins) or one of the two high energy diets : high fat diet (HFD : 60kcal% fat, 20kcal% carbohydrates, 20kcal% proteins). The second diet (HFD-KO) differs from the HFD by the substitution of part of fat (18 kcal%) by the Krill oil. At sacrifice, reliable markers for oxidative stress, 7,8 dihydro 8oxo 2deoxygua-nosine (8 OH Gua), 8iso PGF2alpha, malondialdehyde (MDA) and protein carbonyl levels were measured in liver, abdominal adipose tissue (AAT) and in the muscle. In addition, antioxidant capacity was determined by calculating total glutathione level and catalase and SOD activity in the latter tissues. Results The HF diet induced oxidative stress characterized by elevated MDA, carbonyls and 8 isoPGF2alpha contents and DNA damage as indicated by a higher 8OH Gua levels with a decrease of antioxidant defense (SOD, CAT, Glutathione). The KO treated-rats liver and AAT medium displayed a significant decrease in 8 – iso PGF2alpha, MDA and protein carbonyl levels and an increased SOD, CAT activity and total glutathione content compared to HFD. However the latter group muscle revealed a higher total glutathione levels and a slight decrease in MDA and 8 iso-PG2alpha levels while the catalase activity increased after the enrichment with the KO. The 8OHGua levels were significantly lower in the liver and AAT KO supplemented group as compared to HFD but this parameter was not affected in muscle. Conclusions Krill oil may be a therapeutic useful compound by preserving antioxidant mechanisms and protecting cellular components of insulin resistant-related-several peroxidative damages.

P2-13: The therapeutic effects of dietary krill oil (euphausia superba) supplementation on serum oxidative stress and DNA damages markers in cafeteria-diet-overfed rats

Background The prevalence of obesity has increased dramatically in recent decades, so have the risks of associated medical conditions, such as type 2 diabete and cardiovascular disease, raising serious concerns for public health. Obesity is encouraged by current obesogenic environmental conditions that promote the intake of high-energy-dense foods and increased portion sizes. Cafeteria animal models provide a useful tool to study the metabolic syndrome in humans. Several animal studies and clinical trials suggest that marine bioactive oils supply may have potential effects on obesity and its associated features. Thus, the aim of this study was to evaluate the effects of krill oil enrichment in cafeteria-diet-overfed rats and their capacity to respond to acute changes on some antioxidant/ oxidant markers. Methods Eighteen aging male Wistar rats were divided into three groups of six each and were exposed for the ensuing 8 weeks to one of the diets : control group (C) which was submitted to standard chow (330kcal/100g), containing 24% of proteins, 5% of lipids and 70% of carbohydrates. Cafeteria standard group (CS) exposed to cafeteria diet (420kcal/100 g) containing 30 g of standard chow and 30 g of sausage-dry cookies mixture, cheese, chips, chocolate, and peanuts in proportions of 2:2:2: 1:1:1. The last group received a cafeteria diet enriched in oral force-feeding krill oil 2% (KO-CS). Results Despite modest differences in body weight, cafeteria-fed animals underwent an exacerbated body fat accumulation and increased metabolic risk. The substitution of standard chow diet by the cafeteria diet induced several disturbances in term of metabolic response to the radical attack in key tissues involved in antioxidant defense as demonstrated by the increase of TBARS, 8-OHdG DNA damages marker and isoprostanes levels in cafeteria-diet-fed rats. The serum TBARS, 8-OHdG and isoprostanes levels were significantly lowered by 45% and 25% respectively in the in the KO-CS group compared to CS group. Serum uric acid and albumin contents were decreased respectively by 36% and 18% in the krill oil enriched CS group as compared to cafeteria group. Conclusions A short period of exposure to a cafeteria diet in is enough to disturb the metabolic response to the radical attack in key tissues involved in antioxidant defense. The important antioxidant activity of KO could probably be due to its bioactive compounds (n-3 PUFA, phenolic compounds, alpha-tocopherol, manganese). Thus, its incorporation in a dietetic program can be strategically effective for the prevention/management, indeed improvement of free radical attack in obese subjects, which will prevent the obesity complications.