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Adipose tissue nutrigenomic study in Iberian pigs with dietary intervention of oleic acid supplementation

ABSTRACT: We studied the influence of the oleic acid content of the diet on adipose tissue transcriptome. Iberian pigs were fed a standard (C) or a high oleic sunflower oil enriched (HO) diet. Transcriptome analyses were performed in adipose tissue samples (inner layer) obtained at slaughter (110 kg live weight) employing the Affymetrix porcine GeneChip. Normalized and filtered microarray expression data (background corrected and base-2 logarithmic-transformed) were analyzed through Bayesian inference using the GEAMM v.1.6 program. Statistically significant expression differences (FDR<0.10) between C and HO groups were observed for a total of ten probes corresponding to nine different known genes. Six genes were overexpressed in the HO group and three were overexpressed in the C group. Expression differences between groups ranged from 1.38 to 2.75-fold. The two most significantly DE genes were related with immune defense (TCRB and GPR183) and others were related with nutrient metabolism as glicerolipid metabolism (GK), phospholipid and sphingolipid metabolism (PPM1L), carbohydrate metabolism (FBP2) aminoacid metabolism and energy homeostasis (PRSS35 and CKB) and gene expression regulation and adipogenesis (RXRG).

ORGANISM(S): Sus scrofa

PROVIDER: GSE47941 | GEO | 2013/06/14

SECONDARY ACCESSION(S): PRJNA208407

REPOSITORIES: GEO

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Adipose tissue nutrigenomic study in Iberian pigs with dietary intervention of oleic acid supplementation

Project description:We studied the influence of the oleic acid content of the diet on adipose tissue transcriptome. Iberian pigs were fed a standard (C) or a high oleic sunflower oil enriched (HO) diet. Transcriptome analyses were performed in adipose tissue samples (inner layer) obtained at slaughter (110 kg live weight) employing the Affymetrix porcine GeneChip. Normalized and filtered microarray expression data (background corrected and base-2 logarithmic-transformed) were analyzed through Bayesian inference using the GEAMM v.1.6 program. Statistically significant expression differences (FDR<0.10) between C and HO groups were observed for a total of ten probes corresponding to nine different known genes. Six genes were overexpressed in the HO group and three were overexpressed in the C group. Expression differences between groups ranged from 1.38 to 2.75-fold. The two most significantly DE genes were related with immune defense (TCRB and GPR183) and others were related with nutrient metabolism as glicerolipid metabolism (GK), phospholipid and sphingolipid metabolism (PPM1L), carbohydrate metabolism (FBP2) aminoacid metabolism and energy homeostasis (PRSS35 and CKB) and gene expression regulation and adipogenesis (RXRG). 15 Iberian castrated male pigs were adscribed to one of two experimental groups at 28 kg live weight (7 animals in Control group and 8 animals in High Oleic group). Nutritional treatment was maintained until sacrifice of the animals at 110 kg of live weight. At the sacrifice, backfat adipose tissue was sampled from each animal at the level of the last rib.

2013-06-14 | E-GEOD-47941 | biostudies-arrayexpress

Oxysterol Sensing through GPR183 Triggers Endothelial Senescence and Cardio-renal Injuries via Altering Circadian Signaling in Hypertension

Project description:Background: Despite endothelial dysfunction being considered as the initial step of the development of hypertension and associated cardio-renal syndromes, effective therapeutic strategies to prevent endothelial injuries are still lacking. GPR183 is a recently identified GPCR for oxysterols and hydroxylated metabolites of cholesterol. Here, we explored a previously unappreciated role of GPR183 in hypertension and age-related cardio-renal injuries. Methods and results: Mice were treated with DOCA/Salt or AngII to induce hypertension. we found that endothelial GPR183 was significantly induced in aged or hypertensive mice, which was further confirmed in renal biopsies from elderly people or subjects with hypertensive nephropathy. In addition, we found that endothelial-specific GPR183 deletion markedly ameliorated endothelial senescence and cardio-renal injuries in hypertensive mice. Mechanistically, we found that GPR183 disrupted circadian signaling by inhibiting PER1 expression, thereby facilitating endothelial senescence and dysfunction through the cAMP/PKA/CREB signaling pathway. Importantly, pharmacological inhibition of the oxysterol-GPR183 axis by NIBR189 or Clotrimazole ameliorated endothelial senescence and cardio-renal injuries in hypertensive mice. Conclusions: GPR183 is an attractive therapeutic target for hypertension and age-related diseases. Targeting GPR183 could provide novel strategies for managing hypertension and its associated cardio-renal injuries.

2024-06-23 | GSE270175 | GEO

FBP2 inhibits sarcoma progression by restraining mitochondrial biogenesis

Project description:We show that expression of the gluconeogenic isozyme fructose-1,6-bisphosphatase 2 (FBP2) is silenced in a broad spectrum of soft tissue sarcoma (STS) subtypes, revealing an apparent common metabolic feature shared by diverse STS. Enforced FBP2 expression inhibits STS cell and tumor growth through two distinct mechanisms. First, cytosolic FBP2 antagonizes elevated glycolysis associated with the “Warburg effect”, thereby inhibiting sarcoma cell proliferation. Second, nuclear-localized FBP2 restrains mitochondrial biogenesis and respiration in a catalytic activity-independent manner by inhibiting the expression of nuclear respiratory factor (NRF1) and mitochondrial transcription factor A (TFAM). Specifically, nuclear FBP2 colocalizes with the c-Myc transcription factor at the TFAM locus and represses c-Myc-dependent TFAM expression. This unique dual function of FBP2 provides a rationale for its selective suppression in STS, identifying a potential metabolic vulnerability and possible therapeutic target. This study aims to globally compare the transcriptomes from control or FBP2-expressing LPS246 cells. Total RNA was isolated from 5 sets of control cells and 5 sets of FBP2-expressing cells using RNeasy Mini Kit (Qiagen). Low-throughput library prep using Illumina truSeq stranded mRNA kit. The sequencing were performed on Illumina Platform 100SR, with 312 million raw reads/sample.

2019-09-20 | GSE137755 | GEO

Analyzing the impact of Mycobacterium tuberculosis infection on primary human macrophages

Project description:The success of Mycobacterium tuberculosis (Mtb) as pathogen is tightly linked to its ability to recalibrate host metabolic processes in infected host macrophages. Correspondingly, analysis of RNA-sequencing datasets showed altered gene expression of key metabolic enzymes involved in NAD+, creatine, glucose and glutamine metabolism (e.g NAMPT, IDO1, SLC6A8, CKB, HK2) in Mtb-infected M2 macrophages.

2020-04-16 | GSE148731 | GEO

ANGPTL4 binds to leptin receptor to regulate ectopic bone formation and fat metabolism

Project description:Leptin protein was thought to be unique to leptin receptor (LepR), but the phenotypes of mice with mutation in LepR (db/db) and leptin (ob/ob) are not identical, and the cause remains unclear. Here, we show that db/db, but not ob/ob mice had defect in tenotomy-induced heterotopic ossification (HO), implicating alternative ligand(s) for LepR might be involved. Ligand screening revealed that ANGPTL4, a stress and fasting-induced factor, was elicited from brown adipose tissue after tenotomy, bound to LepR on PRRX1+ mesenchymal cells at the HO cite, thus promotes chondrogenesis and HO development. Disruption of LepR in PRRX1+ cells, or lineage ablation of LepR+ cells, or deletion of ANGPTL4 impeded chondrogenesis and HO in mice. Surprisingly, exogenous ANGPTL4 treatment not only promoted HO, but facilitated the transformation from white to brown adipose tissue in mice. These findings identify ANGPTL4 as a novel ligand for LepR to stimulate HO and regulate fat metabolism.

2024-07-03 | PXD043087 | Pride

Krill oil supplementation in vivo promotes increased fuel metabolism and protein synthesis in cultured human skeletal muscle cells

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

Transcription profiling of wild type, sco1 and sco2 knock out mutants of S. cerevisiae BY4741 in early response to different doses of oleic acid

Project description:This experiment describes the transcriptional response to oleic acid as a sole carbon source of yeast strains differing in their respiratory competence: the BY4741 wild type strain is considered as normal, sco1 knock out mutant is respiratory deficient and sco2 knock out mutant has a better respiratory competence then the wild type strain. The three strains underwent metabolic shift from 2% glucose as a carbon source to oleic acid at both standard (0.1%) and high (5%) concentration. The transcriptional profiling comprises two time points after metabolic shift: 2 hours and 5 hours. mRNA levels were compared with reference growth condition: exponential phase in 2% glucose. The purpose of this experiment is to gain deeper insight in the relationship between fatty acid metabolism and respiratory metabolism.

2011-01-31 | E-TABM-614 | biostudies-arrayexpress

The HIF-1α/PLOD2 axis integrates extracellular matrix organization and cell metabolism leading to aberrant musculoskeletal repair.

Project description:While hypoxic signaling has been shown to play a role in many cellular processes, its role in metabolism linked extracellular matrix (ECM) organization and downstream processes of cell fate after musculoskeletal injury remains to be determined. Heterotopic ossification (HO) is a debilitating condition where abnormal bone formation occurs within extra-skeletal tissues. Hypoxia and hypoxia-inducible factor 1α (HIF-1α) activation have been shown to promote HO. However, the underlying molecular mechanisms by which the HIF-1α pathway in mesenchymal progenitor cells (MPCs) contributes to pathologic bone formation remain to be elucidated. Here we used a proven mouse injury-induced HO model to investigate the role of HIF-1α on aberrant cell fate. Using single-cell RNA-sequencing (scRNA-Seq), we found that collagen ECM organization is the most highly up-regulated biological process in MPCs. Zeugopod mesenchymal cell-specific deletion of Hif1α (Hoxa11-CreERT2; Hif1afl/fl) significantly mitigated HO in vivo. ScRNA-Seq analysis of these Hoxa11-CreERT2; Hif1afl/fl mice identified the PLOD2/LOX pathway for collagen cross-linking as downstream of the HIF-1α regulation of HO. Importantly, our scRNA-seq data and mechanistic studies further uncovered that glucose metabolism in MPCs is most highly impacted by HIF-1α deletion.

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Krill oil supplementation in vivo promotes increased fuel metabolism and protein synthesis in cultured human skeletal muscle cells

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

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