PMCC PMCC

Search tips
Search criteria

Advanced
Results 1-3 (3)
 

Clipboard (0)
None

Select a Filter Below

Journals
Year of Publication
Document Types
author:("eklund, Iris")
1.  Blood cell gene expression associated with cellular stress defense is modulated by antioxidant-rich food in a randomised controlled clinical trial of male smokers 
BMC Medicine  2010;8:54.
Background
Plant-based diets rich in fruit and vegetables can prevent development of several chronic age-related diseases. However, the mechanisms behind this protective effect are not elucidated. We have tested the hypothesis that intake of antioxidant-rich foods can affect groups of genes associated with cellular stress defence in human blood cells. Trial registration number: NCT00520819 http://clinicaltrials.gov.
Methods
In an 8-week dietary intervention study, 102 healthy male smokers were randomised to either a diet rich in various antioxidant-rich foods, a kiwifruit diet (three kiwifruits/d added to the regular diet) or a control group. Blood cell gene expression profiles were obtained from 10 randomly selected individuals of each group. Diet-induced changes on gene expression were compared to controls using a novel application of the gene set enrichment analysis (GSEA) on transcription profiles obtained using Affymetrix HG-U133-Plus 2.0 whole genome arrays.
Results
Changes were observed in the blood cell gene expression profiles in both intervention groups when compared to the control group. Groups of genes involved in regulation of cellular stress defence, such as DNA repair, apoptosis and hypoxia, were significantly upregulated (GSEA, FDR q-values < 5%) by both diets compared to the control group. Genes with common regulatory motifs for aryl hydrocarbon receptor (AhR) and AhR nuclear translocator (AhR/ARNT) were upregulated by both interventions (FDR q-values < 5%). Plasma antioxidant biomarkers (polyphenols/carotenoids) increased in both groups.
Conclusions
The observed changes in the blood cell gene expression profiles suggest that the beneficial effects of a plant-based diet on human health may be mediated through optimization of defence processes.
doi:10.1186/1741-7015-8-54
PMCID: PMC2955589  PMID: 20846424
2.  Tumour formation in multiple intestinal neoplasia (Apc Min/+) mice fed with filtered or unfiltered coffee 
Background
The aetiology of colorectal cancer has strong dietary links, and there may be an association between coffee and colorectal cancer risk.
Objective
To study the effects of filtered (low levels of kahweol/cafestol) and unfiltered (high levels of kahweol/cafestol) coffee on tumour formation in multiple intestinal neoplasia (Apc Min/+) mice.
Design
Apc Min/+ mice (n=11 per group) were fed for 9 weeks with 10% w/w of these two types of coffee. Coffee was served as a dietary ingredient mixed with a semi-synthetic AIN-93G-based diet. Plasma levels of caffeine and paraxanthine were used as compliance markers. At the end of the feeding period intestinal tumour number and size were determined. The levels of β-catenin and cyclin D1, two cell-signalling proteins important to the progression of neoplasia, were also analysed in the tumour tissue.
Results
Plasma caffeine and paraxanthine concentrations were 3.2±1.4 and 1.7±0.4 µmol l−1 in the filtered coffee group and 3.6±2.3 and 1.6±0.6 µmol l−1 in the unfiltered coffee group. The level of plasma xanthines was below detection in the control group. The total number of tumours was equal between the dietary groups: 29 for the control, 30 (p =0.767) for the filtered coffee and 29 (p=0.430) for the unfiltered coffee groups. The levels of β-catenin and cyclin D1 in the nuclear fraction of the tumour tissue were also the same between the groups.
Conclusions
Filtered or unfiltered coffee (10% w/w) does not exert antitumorigenic activity in Apc Min/+ mice or change β-catenin and cyclin D1 signalling in the adenoma tissues. The results suggest that coffee does not change neoplasia progression in this animal model.
doi:10.1080/17482970701757119
PMCID: PMC2606993
ApcMin/+ mice; caffeine; coffee; colon cancer; paraxanthine
3.  Functional COMT Val158Met Polymorphism, Risk of Acute Coronary Events and Serum Homocysteine: The Kuopio Ischaemic Heart Disease Risk Factor Study 
PLoS ONE  2007;2(1):e181.
Background
The role of circulating levels of total homocysteine tHcy in the development of coronary heart disease (CHD) is still under debate. One reason for conflicting results between previous studies on homocysteine and heart diseases could be consequence of different interactions between homocysteine and genes in different study populations. Many genetic factors play a role in folate-homocysteine metabolism, like functional polymorphism (Val108Met) in the Catechol-O-methyltransferase (COMT) gene.
Methodology and Findings
Our aim was to examine the role of COMT Val158Met polymorphism and interaction of this polymorphism with serum tHcy and folate concentration on the risk of acute coronary and events in middle-aged men from eastern Finland. A population-based prospective cohort of 792 men aged 46–64 years was examined as part of the Kuopio Ischaemic Heart Disease Risk Factor Study. During an average follow-up of 9.3 years, there were 69 acute coronary events in men with no previous history of CHD. When comparing the COMT low activity genotype with the others, we found an age and examination year adjusted hazard rate ratio (HRR) of 1.73 (95% confidence interval (CI), 1.07–2.79), and an age, examination year, serum LDL and HDL cholesterol, and triglyceride concentration, systolic blood pressure and smoking adjusted HRR of 1.77 (95% CI, 1.05–2.77). Although serum tHcy concentration was not statistically significantly associated with acute coronary events (HRR for the highest third versus others 1.52, 95% CI, 0.93–2.49), subjects with both high serum tHcy and the COMT low activity genotype had an additionally increased adjusted risk of HRR 2.94 (95% CI 1.50–5.76) as compared with other men.
Conclusions
This prospective cohort study suggests that the functional COMT Val158Met polymorphism is associated with increased risk of acute coronary events and it may interact with high serum tHcy levels.
doi:10.1371/journal.pone.0000181
PMCID: PMC1779620  PMID: 17264883

Results 1-3 (3)