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Impaired barrier function by dietary fructo-oligosaccharides (FOS) in rats is accompanied by increased colonic mitochondrial gene expression.

Rodenburg W, Keijer J, Kramer E, Vink C, van der Meer R, Bovee-Oudenhoven IM - BMC Genomics (2008)

Bottom Line: The mechanism responsible for this adverse effect of FOS is unclear.FOS significantly increased expression of 177 mitochondria-related genes.These results indicate that dietary FOS influences intestinal mucosal energy metabolism.

View Article: PubMed Central - HTML - PubMed

Affiliation: TI Food and Nutrition, Wageningen, The Netherlands. wendy.rodenburg@rivm.nl

ABSTRACT

Background: Dietary non-digestible carbohydrates stimulate the gut microflora and are therefore presumed to improve host resistance to intestinal infections. However, several strictly controlled rat infection studies showed that non-digestible fructo-oligosaccharides (FOS) increase, rather than decrease, translocation of Salmonella towards extra-intestinal sites. In addition, it was shown that FOS increases intestinal permeability already before infection. The mechanism responsible for this adverse effect of FOS is unclear. Possible explanations are altered mucosal integrity due to changes in tight junctions or changes in expression of defense molecules such as antimicrobials and mucins. To examine the mechanisms underlying weakening of the intestinal barrier by FOS, a controlled dietary intervention study was performed. Two groups of 12 rats were adapted to a diet with or without FOS. mRNA was collected from colonic mucosa and changes in gene expression were assessed for each individual rat using Agilent rat whole genome microarrays.

Results: Among the 997 FOS induced genes we observed less mucosal integrity related genes than expected with the clear permeability changes. FOS did not induce changes in tight junction genes and only 8 genes related to mucosal defense were induced by FOS. These small effects are unlikely the cause for the clear increase in intestinal permeability that is observed. FOS significantly increased expression of 177 mitochondria-related genes. More specifically, induced expression of genes involved in all five OXPHOS complexes and the TCA cycle was observed. These results indicate that dietary FOS influences intestinal mucosal energy metabolism. Furthermore, increased expression of 113 genes related to protein turnover, including proteasome genes, ribosomal genes and protein maturation related genes, was seen. FOS upregulated expression of the peptide hormone proglucagon gene, in agreement with previous studies, as well as three other peptide hormone genes; peptide YY, pancreatic polypeptide and cholecystokinin.

Conclusion: We conclude that altered energy metabolism may underly colonic barrier function disruption due to FOS feeding in rats.

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Related in: MedlinePlus

Mucosal scrapings (pool of n = 12 per group) were examined for complex IV subunit COXII protein levels. The experiment was performed three times with independent, pools, showing a 1.5; 1.7 and 2.7 fold difference in COXII protein expression relative to Actin, respectively. The 1.5 fold increase is shown.
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Figure 3: Mucosal scrapings (pool of n = 12 per group) were examined for complex IV subunit COXII protein levels. The experiment was performed three times with independent, pools, showing a 1.5; 1.7 and 2.7 fold difference in COXII protein expression relative to Actin, respectively. The 1.5 fold increase is shown.

Mentions: To substantiate the FOS induced transcriptional modulation of mitochondrial genes at the protein level, we analyzed pooled mucosal scrapings of all rats (n = 12 per group). The small increase in mRNA levels of complex IV subunits (~1.4 fold), was confirmed by a similar increase (1.5, 1.7 and 2.7 fold in independent pools, relative to actin) in protein levels of complex IV subunit COX II in the FOS group compared with the control group in pooled (n = 12) mucosal scrapings (Figure 3).


Impaired barrier function by dietary fructo-oligosaccharides (FOS) in rats is accompanied by increased colonic mitochondrial gene expression.

Rodenburg W, Keijer J, Kramer E, Vink C, van der Meer R, Bovee-Oudenhoven IM - BMC Genomics (2008)

Mucosal scrapings (pool of n = 12 per group) were examined for complex IV subunit COXII protein levels. The experiment was performed three times with independent, pools, showing a 1.5; 1.7 and 2.7 fold difference in COXII protein expression relative to Actin, respectively. The 1.5 fold increase is shown.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2311291&req=5

Figure 3: Mucosal scrapings (pool of n = 12 per group) were examined for complex IV subunit COXII protein levels. The experiment was performed three times with independent, pools, showing a 1.5; 1.7 and 2.7 fold difference in COXII protein expression relative to Actin, respectively. The 1.5 fold increase is shown.
Mentions: To substantiate the FOS induced transcriptional modulation of mitochondrial genes at the protein level, we analyzed pooled mucosal scrapings of all rats (n = 12 per group). The small increase in mRNA levels of complex IV subunits (~1.4 fold), was confirmed by a similar increase (1.5, 1.7 and 2.7 fold in independent pools, relative to actin) in protein levels of complex IV subunit COX II in the FOS group compared with the control group in pooled (n = 12) mucosal scrapings (Figure 3).

Bottom Line: The mechanism responsible for this adverse effect of FOS is unclear.FOS significantly increased expression of 177 mitochondria-related genes.These results indicate that dietary FOS influences intestinal mucosal energy metabolism.

View Article: PubMed Central - HTML - PubMed

Affiliation: TI Food and Nutrition, Wageningen, The Netherlands. wendy.rodenburg@rivm.nl

ABSTRACT

Background: Dietary non-digestible carbohydrates stimulate the gut microflora and are therefore presumed to improve host resistance to intestinal infections. However, several strictly controlled rat infection studies showed that non-digestible fructo-oligosaccharides (FOS) increase, rather than decrease, translocation of Salmonella towards extra-intestinal sites. In addition, it was shown that FOS increases intestinal permeability already before infection. The mechanism responsible for this adverse effect of FOS is unclear. Possible explanations are altered mucosal integrity due to changes in tight junctions or changes in expression of defense molecules such as antimicrobials and mucins. To examine the mechanisms underlying weakening of the intestinal barrier by FOS, a controlled dietary intervention study was performed. Two groups of 12 rats were adapted to a diet with or without FOS. mRNA was collected from colonic mucosa and changes in gene expression were assessed for each individual rat using Agilent rat whole genome microarrays.

Results: Among the 997 FOS induced genes we observed less mucosal integrity related genes than expected with the clear permeability changes. FOS did not induce changes in tight junction genes and only 8 genes related to mucosal defense were induced by FOS. These small effects are unlikely the cause for the clear increase in intestinal permeability that is observed. FOS significantly increased expression of 177 mitochondria-related genes. More specifically, induced expression of genes involved in all five OXPHOS complexes and the TCA cycle was observed. These results indicate that dietary FOS influences intestinal mucosal energy metabolism. Furthermore, increased expression of 113 genes related to protein turnover, including proteasome genes, ribosomal genes and protein maturation related genes, was seen. FOS upregulated expression of the peptide hormone proglucagon gene, in agreement with previous studies, as well as three other peptide hormone genes; peptide YY, pancreatic polypeptide and cholecystokinin.

Conclusion: We conclude that altered energy metabolism may underly colonic barrier function disruption due to FOS feeding in rats.

Show MeSH
Related in: MedlinePlus