Project description:Endurance-trained athletes have high oxidative capacity, enhanced insulin sensitivity, and high intracellular lipid accumulation in muscle. These characteristics are likely due to altered gene expression levels in muscle. We used microarrays to detect gene expression profile in endurance-trained athlete skeletal muscle.
Project description:Exercise is beneficial to human’s health, and many of the effects are mediated by changes in immune function. However, the mechanisms underpinning the immune-regulatory effect of exercise remain unclear. We used microarrays to assess the global gene expression in blood leukocytes in young endurance athletes and non-athlete controls, the differential gene expression between two groups was analzyed using bioinformatic methods and enriched biological processes and pathways were identified for up- and down-regulated genes in athletes.
Project description:The aim of the current study was to characterize the genetic adaptive pathways altered by exercise in veteran athletes and age-matched untrained individuals. Two groups of 50-60 year old males: competitive cyclists and untrained, minimally active individuals were examined. All participants completed an acut bout of submaximal endurance exercise and blood samples pre- and post-exercise were analyzed for gene expression changes utilizing genome-wide DNA microarray analysis. Our results indicate distinct differences in gene expression involving energy metabolism, lipids, insuling signaling and cardiovascular function between the two groups. These findings may lead to new insights into beneficial signaling pathways of healthy aging and help identify surrogate markers for monitoring exercise and training load. Blood samples from the control and athlete groups were analyzed at three time-points: T1 (before exercise); T2 (immediately after exercise) and T3 (24 hours after exercise). There were n = 4 samples in each of control and athlete group at T1 and T3; and n = 7 for control group and n = 8 for athlete group at T2. One athlete sample (Sample # 010201) at time - point T2 had a technical replicate.
Project description:Opioids such as morphine have many beneficial properties as analgesics, however, opioids may induce multiple adverse gastrointestinal symptoms. We have recently demonstrated that morphine treatment results in significant disruption in gut barrier function leading to increased translocation of gut commensal bacteria. However, it is unclear how opioids modulate the gut homeostasis. By using a mouse model of morphine treatment, we studied effects of morphine treatment on gut microbiome. We characterized phylogenetic profiles of gut microbes, and found a significant shift in the gut microbiome and increase of pathogenic bacteria following morphine treatment when compared to placebo. In the present study, wild type mice (C57BL/6J) were implanted with placebo, morphine pellets subcutaneously. Fecal matter were taken for bacterial 16s rDNA sequencing analysis at day 3 post treatment. A scatter plot based on an unweighted UniFrac distance matrics obtained from the sequences at OTU level with 97% similarity showed a distinct clustering of the community composition between the morphine and placebo treated groups. By using the chao1 index to evaluate alpha diversity (that is diversity within a group) and using unweighted UniFrac distance to evaluate beta diversity (that is diversity between groups, comparing microbial community based on compositional structures), we found that morphine treatment results in a significant decrease in alpha diversity and shift in fecal microbiome at day 3 post treatment compared to placebo treatment. Taxonomical analysis showed that morphine treatment results in a significant increase of potential pathogenic bacteria. Our study shed light on effects of morphine on the gut microbiome, and its role in the gut homeostasis.
Project description:Early life exposure to antibiotics alters the gut microbiome. These alterations lead to changes in metabolic homeostasis and an increase in host adiposity. We used microarrays to identify metabolic genes that may be up- or down-regulated secondary to antibiotic exposure. Low dose antibiotics have been widely used as growth promoters in the agricultural industry since the 1950’s, yet the mechanisms for this effect are unclear. Because antimicrobial agents of different classes and varying activity are effective across several vertebrate species, we hypothesized that such subtherapeutic administration alters the population structure of the gut microbiome as well as its metabolic capabilities. We generated a model of adiposity by giving subtherapeutic antibiotic therapy (STAT) to young mice and evaluated changes in the composition and capabilities of the gut microbiome. STAT administration increased adiposity in young mice and altered hormones related to metabolism. We observed substantial taxonomic changes in the microbiome, changes in copies of key genes involved in the metabolism of carbohydrates to short-chain fatty acids (SCFA), increases in colonic SCFA levels, and alterations in the regulation of hepatic metabolism of lipids and cholesterol. In this model, we demonstrate the alteration of early life murine metabolic homeostasis through antibiotic manipulation. C57BL6 mice were divided into low-dose penicillin or control groups. Given antibiotics via drinking water after weaning. Sacrificed and liver sections collected for RNA extraction.