Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA141341 | ENA |
REPOSITORIES: ENA
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Project description:Dietary supplementation with ω-3 polyunsaturated fatty acids (ω-3 PUFAs), specifically the fatty acids docosahexaenoic acid (DHA; 22:6 ω-3) and eicosapentaenoic acid (EPA; 20:5 ω-3), is known to have beneficial health effects including improvements in glucose and lipid homeostasis and modulation of inflammation. To evaluate the efficacy of two different sources of ω-3 PUFAs, we performed gene expression profiling in the liver of mice fed diets supplemented with either fish oil or krill oil. We found that ω-3 PUFA supplements derived from a phospholipid krill fraction (krill oil) downregulated the activity of pathways involved in hepatic glucose production as well as lipid and cholesterol synthesis. The data also suggested that krill oil-supplementation increases the activity of the mitochondrial respiratory chain. Surprisingly, an equimolar dose of EPA and DHA derived from fish oil modulated fewer pathways than a krill oil-supplemented diet and did not modulate key metabolic pathways regulated by krill oil, including glucose metabolism, lipid metabolism and the mitochondrial respiratory chain. Moreover, fish oil upregulated the cholesterol synthesis pathway, which was the opposite effect of krill supplementation. Neither diet elicited changes in plasma levels of lipids, glucose or insulin, probably because the mice used in this study were young and were fed a low fat diet. Further studies of krill oil supplementation using animal models of metabolic disorders and/or diets with a higher level of fat may be required to observe these effects.
2011-07-22 | GSE29572 | GEO
Project description:Dietary supplementation with ω-3 polyunsaturated fatty acids (ω-3 PUFAs), specifically the fatty acids docosahexaenoic acid (DHA; 22:6 ω-3) and eicosapentaenoic acid (EPA; 20:5 ω-3), is known to have beneficial health effects including improvements in glucose and lipid homeostasis and modulation of inflammation. To evaluate the efficacy of two different sources of ω-3 PUFAs, we performed gene expression profiling in the liver of mice fed diets supplemented with either fish oil or krill oil. We found that ω-3 PUFA supplements derived from a phospholipid krill fraction (krill oil) downregulated the activity of pathways involved in hepatic glucose production as well as lipid and cholesterol synthesis. The data also suggested that krill oil-supplementation increases the activity of the mitochondrial respiratory chain. Surprisingly, an equimolar dose of EPA and DHA derived from fish oil modulated fewer pathways than a krill oil-supplemented diet and did not modulate key metabolic pathways regulated by krill oil, including glucose metabolism, lipid metabolism and the mitochondrial respiratory chain. Moreover, fish oil upregulated the cholesterol synthesis pathway, which was the opposite effect of krill supplementation. Neither diet elicited changes in plasma levels of lipids, glucose or insulin, probably because the mice used in this study were young and were fed a low fat diet. Further studies of krill oil supplementation using animal models of metabolic disorders and/or diets with a higher level of fat may be required to observe these effects. Twenty-one microarrays: three diets (CO, FO, KO) x seven mice per diet x one microarray per mouse
2011-07-21 | E-GEOD-29572 | biostudies-arrayexpress
Project description:Omega - 3 fatty acids of marine origin exert beneficial effects on lipid metabolism and can protect against insulin resistance in high fat diet (HFD)-fed animals. Simultaneously, recent studies showed that different lipid forms could have numerous consequences regarding the regulation of energy balance, nutrient absorption, and substrate metabolism. Indeed, when omega-3 was provided as triglycerides (TG, i.e. fish oil), it induced dose-dependently the expression of genes involved in lipid metabolism as well as fatty acid oxidation in small intestine of C57BL/6 mice fed various HFDs. As the underlying mechanism(s) explaining the differences in EPA/DHA bioavailability among various lipid forms of Omega-3 is not entirely clear, we performed a mouse study (n=8 per group) using purified HFDs with control HFD based on corn oil (cHF) and part of the lipids were replaced by omega-3 fish lipids in different forms: as either TG (cHF-F), marine phospholipids (PL; Krill oil, given at two different doses Krill-low (Krill-L) and Krill-high (Krill-H)), and as wax esters in the extract from the zooplankton Calanus finmarchicus (Calanus oil CAL-L representing same omega-3 levels as Krill-L diet). As a healthy control we fed a subset of mice standard chow (STD). All mice were fed their diet for 8 weeks and after sacrifice, whole small intestine was isolated, frozen and used for RNA isolation and microarray gene expression analysis using 8x60K Agilent arrays. Results showed that PL-H versus control cHFc induced specifically metabolic lipid pathways, while TG and PL-L mainly affected cytoskeleton regulation.
2020-07-13 | GSE93151 | GEO
Project description:Krill oil is a dietary supplement derived from Antarctic krill; a small crustacean found in the ocean. Krill oil is a rich source of omega-3 fatty acids, specifically eicosapentaenoic acid and docosahexaenoic acid, as well as the antioxidant astaxanthin. The aim of this study was to investigate the effects of krill oil supplementation, compared to placebo oil (high oleic sunflower oil added astaxanthin), in vivo on energy metabolism and substrate turnover in skeletal muscle cells. Skeletal muscle cells (myotubes) were obtained before and after a 7-week krill oil or placebo oil intervention, and glucose and oleic acid metabolism and leucine accumulation, as well as effects of different stimuli in vitro, were studied in the myotubes. In vivo intervention with krill oil increased oleic acid oxidation and leucine accumulation in skeletal muscle cells, however no effects were observed on glucose metabolism. The krill oil-intervention-induced increase in oleic acid oxidation correlated negatively with changes in serum low-density lipoprotein (LDL) concentration. In addition, myotubes were also exposed to krill oil in vitro. The in vitro study revealed that 24 h of krill oil treatment increased both glucose and oleic acid metabolism, enhancing energy substrate utilization. Transcriptomic analysis comparing myotubes obtained before and after krill oil-supplementation identified differentially expressed genes associated with e.g. glycolysis/gluconeogenesis, metabolic pathways and calcium signaling pathway, while proteomic analysis demonstrated upregulation of e.g. LDL-receptor in myotubes obtained after krill oil intervention. These findings suggest that krill oil intervention promotes increased fuel metabolism and protein synthesis in human skeletal muscle cells, with potential implications for metabolic health.
2024-11-20 | GSE278505 | GEO
Project description:Krill oil is a dietary supplement derived from Antarctic krill; a small crustacean found in the ocean. Krill oil is a rich source of omega-3 fatty acids, specifically eicosapentaenoic acid and docosahexaenoic acid, as well as the antioxidant astaxanthin. The aim of this study was to investigate the effects of krill oil supplementation, compared to placebo oil (high oleic sunflower oil added astaxanthin), in vivo on energy metabolism and substrate turnover in skeletal muscle cells. Skeletal muscle cells (myotubes) were obtained before and after a 7-week krill oil or placebo oil intervention, and glucose and oleic acid metabolism and leucine accumulation, as well as effects of different stimuli in vitro, were studied in the myotubes. In addition, myotubes were also exposed to krill oil in vitro. The in vitro study revealed that 24 h of krill oil treatment increased both glucose and oleic acid metabolism, enhancing energy substrate utilization. In vivo intervention with krill oil increased oleic acid oxidation and leucine accumulation in skeletal muscle cells, however no effects were observed on glucose metabolism. The krill oil-intervention-induced increase in oleic acid oxidation correlated negatively with changes in serum low-density lipoprotein (LDL) concentration. Transcriptomic analysis comparing myotubes obtained before and after krill oil-supplementation identified differentially expressed genes associated with e.g. glycolysis/gluconeogenesis, metabolic pathways and calcium signaling pathway, while proteomic analysis demonstrated upregulation of e.g. LDL-receptor. These findings suggest that krill oil intervention promotes increased fuel metabolism and protein synthesis in human skeletal muscle cells, with potential implications for metabolic health.
2024-10-14 | PXD052661 | Pride
Project description:Dietary effects of arachidonate-rich fungal oil and fish oil on murine hepatic and hippocampal gene expression.<BR> <LI><u>Brain:</u></LI><BR> GSM2558: Control<bR> GSM2559: Control <bR> GSM2560: Fungal oil (AA)<bR> GSM2561: Fungal oil (AA)<bR> GSM2562: Fish oil (DHA)<bR> GSM2563: Fish oil (DHA)<bR> GSM2564: Fish and Fungal oil (DHA + AA)<bR> <LI><u>Liver:</u></LI><bR> GSM2565: Control <bR> GSM2566: Control<bR> GSM2567: Control<bR> GSM2568: Control<bR> GSM2569: Fungal oil (AA)<bR> GSM2570: Fungal oil (AA)<bR> GSM2571: Fish oil (DHA)<bR> GSM2572: Fish oil (DHA)<bR> GSM2573: Fish + Fungal oil (DHA +AA)<bR> GSM2574: Fish + Fungal oil (DHA +AA)<bR> Keywords: ordered
2002-11-11 | GSE91 | GEO
Project description:Dietary effects of arachidonate-rich fungal oil and fish oil on murine hepatic and hippocampal gene expression.; Brain:; GSM2558: Control; GSM2559: Control ; GSM2560: Fungal oil (AA); GSM2561: Fungal oil (AA); GSM2562: Fish oil (DHA); GSM2563: Fish oil (DHA); GSM2564: Fish and Fungal oil (DHA + AA); Liver:; GSM2565: Control ; GSM2566: Control; GSM2567: Control; GSM2568: Control; GSM2569: Fungal oil (AA); GSM2570: Fungal oil (AA); GSM2571: Fish oil (DHA); GSM2572: Fish oil (DHA); GSM2573: Fish + Fungal oil (DHA +AA); GSM2574: Fish + Fungal oil (DHA +AA)
2007-12-13 | E-GEOD-91 | biostudies-arrayexpress
Project description:There is accumulating evidence that interfering with the basic aging mechanisms can enhance healthy longevity. Many cellular processes contribute to aging and are referred to as “hallmarks of aging”; by presumption, interventional/therapeutic strategies targeting on multiple ageing hallmarks could be more effective to delay ageing than targeting on one hallmark. While the health-promoting qualities of marine oils have been extensively studied, the underlying molecular mechanisms are not fully understood. Lipid extracts from Antarctic krill are rich in long-chain omega-3 fatty acids (eicosapentaenoic acid/EPA and docosahexaenoic acid/DHA), choline, and astaxanthin. Here, we investigated whether krill oil promotes healthy aging in the small roundworm C. elegans. We show that krill oil rewires distinct gene expression programs that contribute to attenuate several aging hallmarks, including oxidative stress, proteotoxic stress, senescence, genomic instability, and mitochondrial dysfunction. In a C. elegans model of Parkinson´s disease, krill oil protects dopaminergic neurons from aging-related degeneration, decreases alpha synuclein aggregation, and improves dopamine-dependent behavior and cognition. Mechanistically, krill oil increases neuronal resilience through temporal transcriptome rewiring to promote anti-oxidative stress and inflammation via healthspan regulating transcription factors such as SNK-1. However, also krill oil promotes DA neuron survival through regulation of synaptic transmission and neuronal functions via PBO-2 and RIM-1. Collectively, krill oil rewires global gene expression programs and promotes healthy aging via abrogating multiple ageing hallmarks, shedding light on further pre-clinical and clinical explorations.
2022-11-30 | GSE207152 | GEO
Project description:Acetaminophen is a widely used antipyretic and analgesic drug, and its overdose is the leading cause of drug-induced acute liver failure. This study aimed to investigate the effect and mechanism of Lacticaseibacillus casei Shirota (LcS), an extensively used and highly studied probiotic, on acetaminophen-induced acute liver injury. C57BL/6 mice were gavaged with LcS suspension or saline once daily for 7 days before the acute liver injury was induced via intraperitoneal injection of 300 mg/kg acetaminophen. The results showed that LcS significantly decreased acetaminophen-induced liver and ileum injury, as demonstrated by reductions in the increases in aspartate aminotransferase, total bile acids, total bilirubin, indirect bilirubin and hepatic cell necrosis. Moreover, LcS alleviated the acetaminophen-induced intestinal mucosal permeability, elevation in serum IL-1α and lipopolysaccharide, and decreased levels of serum eosinophil chemokine (eotaxin) and hepatic glutathione levels. Furthermore, analysis of the gut microbiota and metabolome showed that LcS reduced the acetaminophen-enriched levels of Cyanobacteria, Oxyphotobacteria, long-chain fatty acids, cholesterol and sugars in the gut. Additionally, the transcriptome and proteomics showed that LcS mitigated the downregulation of metabolism and immune pathways as well as glutathione formation during acetaminophen-induced acute liver injury. This is the first study showing that pretreatment with LcS alleviates acetaminophen-enriched acute liver injury, and it provides a reference for the application of LcS.
2023-07-26 | PXD044099 |