Determining Energy Needs in Colorectal Cancer
Ontology highlight
ABSTRACT:
DISEASE(S): Colorectal Cancer,Colorectal Neoplasms
PROVIDER: 2242749 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
Similar Datasets
Project description:Lipoprotein Lipase Overexpression in Skeletal Muscle Attenuates Weight Regain by Potentiating Energy Expenditure
| PRJNA647913 | ENA
Project description:Insulin is a potent pleiotropic hormone that affects processes such as cellular growth, differentiation, apoptosis, ion flux, energy expenditure, and carbohydrate, lipid, and protein metabolism. We used microarrays to detail the global programme of gene expression underlying the influence of insulin in human skeletal muscle collected from different human individuals including 20 insulin sensitive, 20 insulin resistant and 15 diabetic patients. We identified distinct classes of up-regulated and down-regulated genes during these processes. The pathophysiology of obesity represents an imbalance between a high energy intake and/or low energy expenditure. Resting energy expenditure (REE) comprises 60-75% of total energy expenditure. The respiratory quotient (RQ) is used to estimate fuel partitioning between fat and carbohydrate as preferred substrates for energy generation, and fuel preferences to generate REE also exhibit individual variation. Genes influencing REE and RQ could represent candidate genes for obesity, Metabolic Syndrome, and Type 2 Diabetes due to the involvement of these traits in energy balance and substrate oxidation. We used microarrays to explore the molecular bases for individual variation in REE and fuel partitioning as reflected by RQ. We performed microarray studies in human vastus lateralis muscle biopsies from 40 healthy subjects with measured REE and RQ values. We identified genes significantly correlated with REE and RQ, respectively. Human skeletal muscle samples were biopsied from different individuals before and after insulin treatment for RNA extraction and hybridization on Affymetrix microarrays.
2010-07-08 | E-GEOD-22309 | biostudies-arrayexpress
Project description:Skeletal muscle plays a central role in the control of metabolism and exercise tolerance. Analysis of muscle enhancers activated after exercise in mice revealed the orphan nuclear receptor NURR1/NR4A2 as a prominent component of exercise-responsive enhancers. We show that exercise enhances the expression of NURR1 and transgenic overexpression of NURR1 in skeletal muscle confers an endurance phenotype in mice. NURR1 expression in skeletal muscle is also sufficient to prevent hyperglycemia and hepatic steatosis by enhancing muscle glucose uptake and storage as glycogen. Furthermore, treatment of obese mice with putative NURR1 agonists increases energy expenditure, improves glucose tolerance, and confers a lean phenotype, mimicking the effects of exercise. These findings identify a key role for NURR1 in governance of skeletal muscle glucose metabolism and reveal a transcriptional link between exercise and metabolism. Our findings also identify NURR1 agonists as possible exercise mimetics with the potential to ameliorate obesity and other metabolic abnormalities.
2019-08-01 | GSE130838 | GEO
Project description:Skeletal muscle plays a central role in the control of metabolism and exercise tolerance. Analysis of muscle enhancers activated after exercise in mice revealed the orphan nuclear receptor NURR1/NR4A2 as a prominent component of exercise-responsive enhancers. We show that exercise enhances the expression of NURR1 and transgenic overexpression of NURR1 in skeletal muscle confers an endurance phenotype in mice. NURR1 expression in skeletal muscle is also sufficient to prevent hyperglycemia and hepatic steatosis by enhancing muscle glucose uptake and storage as glycogen. Furthermore, treatment of obese mice with putative NURR1 agonists increases energy expenditure, improves glucose tolerance, and confers a lean phenotype, mimicking the effects of exercise. These findings identify a key role for NURR1 in governance of skeletal muscle glucose metabolism and reveal a transcriptional link between exercise and metabolism. Our findings also identify NURR1 agonists as possible exercise mimetics with the potential to ameliorate obesity and other metabolic abnormalities.
2019-08-01 | GSE130839 | GEO
Project description:We aimed to investigate the human skeletal muscle (SkM) DNA methylome after exercise in low carbohydrate (CHO) energy balance (with high fat) compared with exercise in low-CHO energy deficit (with low fat) conditions. The objective to identify novel epigenetically regulated genes and pathways associated with ‘train-low sleep-low’ paradigms. The sleep-low conditions included 9 males that cycled to deplete muscle glycogen while reaching a set energy expenditure. Post-exercise, low-CHO meals (protein-matched) completely replaced (using high-fat) or only partially replaced (low-fat) the energy expended. The following morning resting baseline biopsies were taken and the participants then undertook 75 minutes of cycling exercise, with skeletal muscle biopsies collected 30 minutes and 3.5 hours post exercise. Discovery of genome-wide DNA methylation was undertaken using Illumina EPIC arrays and targeted gene expression analysis was conducted by RT-qPCR. At baseline participants under energy balance (high fat) demonstrated a predominantly hypermethylated (60%) profile across the genome compared to energy deficit-low fat conditions. However, post exercise performed in energy balance (with high fat) elicited a more prominent hypomethylation signature 30 minutes post-exercise in gene regulatory regions important for transcription (CpG islands within promoter regions) compared with exercise in energy deficit (with low fat) conditions. Such hypomethylation was enriched within pathways related to: IL6-JAK-STAT signalling, metabolic processes, p53 / cell cycle and oxidative / fatty acid metabolism. Hypomethylation within the promoter regions of genes: HDAC2, MECR, IGF2 and c13orf16 were associated with significant increases in gene expression in the post-exercise period in energy balance compared with energy deficit. Furthermore, histone deacetylase, HDAC11 was oppositely regulated at the gene expression level compared with HDAC2, where HDAC11 was hypomethylated yet increased in energy deficit compared with energy balance conditions. Overall, we identify some novel epigenetically regulated genes associated with train-low sleep-low paradigms.
2023-03-29 | GSE223786 | GEO
Project description:Primary outcome(s): resting energy expenditure and the stress factor on endoscopic operation postoperative day 1
| 2642350 | ecrin-mdr-crc
Project description:The combination of decreasing food intake and increasing energy expenditure represents a powerful strategy for counteracting cardiometabolic diseases, such as obesity and type 2 diabetes1. Yet current approaches require conjugating multiple receptor agonists to achieve both effects2–4 and, thus far, no safe energy-expending option has reached the clinic. Here we show that activation of Neurokinin 2 Receptor (NK2R) is sufficient to suppress appetite centrally and increase energy expenditure peripherally. We focused on NK2R after discovering its genetic links to obesity and glucose control. However, therapeutically exploiting NK2R signalling has previously been unattainable because its endogenous ligand, Neurokinin A (NKA), is short-lived and lacks receptor specificity5,6. Therefore, we developed selective, long-acting NK2R agonists, with potential for once-weekly administration in humans. In mice, these agonists elicit weight loss by inducing energy expenditure and non-aversive appetite suppression that circumvents canonical leptin signalling. Additionally, a hyperinsulinemic-euglycemic clamp reveals that NK2R agonism acutely enhances insulin sensitization. In diabetic, obese nonhuman primates, NK2R activation significantly decreases body weight, blood glucose, triglycerides, and cholesterol, and ameliorates insulin resistance. These findings identify a single receptor target that leverages both energy-expending and appetite-suppressing programs to improve energy homeostasis and reverse cardiometabolic dysfunction across species.
2024-11-27 | GSE276735 | GEO
Project description:Gene expression changes in mouse skeletal muscle were assessed in wild-type and Jhdm2a null skeletal muscle in an effort to define the role of Jhdm2a in energy expenditure and metabolism.
2009-02-05 | GSE13552 | GEO
Project description:Skeletal muscle, as a large and insulin sensitive tissue, is an important contributor to metabolic homeostasis and energy expenditure. Obese dogs exhibit skeletal muscle insulin resistance, but the causes of these changes are unclear. Thus, we used canine microarrays to analyze gene expression profiles of skeletal muscle tissue collected from obese dogs, after 24 wk of ad libitum feeding. Skeletal muscle tissue samples were collected from 9 intact female beagles (4 yr-old; 4 control; 5 ad libitum) after 24 wk of ad libitum feeding.
2012-01-15 | E-GEOD-29279 | biostudies-arrayexpress