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Background One way to improve both the ecological performance and functionality of probiotic bacteria is by combining them with a prebiotic in the form of a synbiotic. However, the degree to which such synbiotic formulations improve probiotic strain functionality in humans has not been tested systematically. Our goal was to use a randomized, double-blind, placebo-controlled, parallel-arm clinical trial in obese humans to compare the ecological and physiological impact of the prebiotic galactooligosaccharides (GOS) and the probiotic strains Bifidobacterium adolescentis IVS-1 (autochthonous and selected via in vivo selection) and Bifidobacterium lactis BB-12 (commercial probiotic allochthonous to the human gut) when used on their own or as synbiotic combinations. After 3 weeks of consumption, strain-specific quantitative real-time PCR and 16S rRNA gene sequencing were performed on fecal samples to assess changes in the microbiota. Intestinal permeability was determined by measuring sugar recovery in urine by GC after consumption of a sugar mixture. Serum-based endotoxin exposure was also assessed. Results IVS-1 reached significantly higher cell numbers in fecal samples than BB-12 ( P  < 0.01) and, remarkably, its administration induced an increase in total bifidobacteria that was comparable to that of GOS. Although GOS showed a clear bifidogenic effect on the resident gut microbiota, both probiotic strains showed only a non-significant trend of higher fecal cell numbers when administered with GOS. Post-aspirin sucralose:lactulose ratios were reduced in groups IVS-1 ( P  = 0.050), IVS-1 + GOS ( P  = 0.022), and GOS ( P  = 0.010), while sucralose excretion was reduced with BB-12 ( P  = 0.002) and GOS ( P  = 0.020), indicating improvements in colonic permeability but no synergistic effects. No changes in markers of endotoxemia were observed. Conclusion This study demonstrated that “autochthony” of the probiotic strain has a larger effect on ecological performance than the provision of a prebiotic substrate, likely due to competitive interactions with members of the resident microbiota. Although the synbiotic combinations tested in this study did not demonstrate functional synergism, our findings clearly showed that the pro- and prebiotic components by themselves improved markers of colonic permeability, providing a rational for their use in pathologies with an underlying leakiness of the gut.

Background Previous studies examining the metabolic consequences of dietary iron deficiency have reported elevated serum glucose concentrations in iron-deficient animals. Importantly, the majority of these findings were observed using an earlier version of a laboratory animal diet (AIN-76A) in which the primary carbohydrate source was sucrose – a disaccharide known to negatively impact both glucose and lipid homeostasis. The AIN-76A diet formula was improved in 1993 (AIN-93) to optimize animal nutrition with a major change being the substitution of cornstarch for sucrose. Therefore, we sought to examine the effects of iron deficiency on steady-state glucose homeostasis and the hepatic expression of glucose- and lipid-related genes in rats fed an iron-deficient diet based on either an AIN-76A or AIN-93 diet. Methods The study design consisted of 6 treatment groups: control (C; 40 mg Fe/kg diet), iron deficient (ID; ≤ 3 mg Fe/kg diet), or pair-fed (PF; 40 mg Fe/kg) fed either an AIN-76A or AIN-93 diet for 21 d. Hemoglobin and hematocrit were measured in whole blood. Serum insulin and cortisol were measure by ELISA. Serum glucose and triacylglycerols were measured by standard colorimetric enzyme assays. Alterations in hepatic gene expression were determined by real-time qPCR. Results Hemoglobin and hematocrit were significantly reduced in both ID groups compared to the C and PF groups. Similarly, animals in the both ID groups exhibited elevated steady-state levels of blood glucose and insulin, and significantly decreased levels of circulating cortisol compared to their respective PF controls. Serum triacyglycerols were only increased in ID animals consuming the AIN-76A diet. Hepatic gene expression analyses revealed a ~4- and 3-fold increase in the expression of glucokinase and pyruvate dehydrogenase kinase-4 mRNA, respectively, in the ID group on either diet compared to their respective PF counterparts. In contrast, the expression of lipogenic genes was significantly elevated in the AIN-76 ID group, while expression of these genes was unaffected by iron status in the AIN-93 ID group. Conclusions These results indicate that an impaired iron status is sufficient to alter glucose homeostasis, though alterations in lipid metabolism associated with ID are only observed in animals receiving the AIN-76A diet.

Background A significant proportion of the eligible population is non-adherent to colonoscopy for colorectal cancer (CRC) screening. Aims To define the demographic and clinical variables associated with non-adherence and multiple cancellations to scheduled colonoscopy within 1 year in a CRC screening and adenomatous polyp surveillance population. Methods This was an observational cohort study of 617 consecutive patients scheduled to undergo colonoscopy at an outpatient academic tertiary care center for CRC screening or adenomatous polyp surveillance from January 2012 to September 2012. Results Overall, 551 patients (89.3 %) were adherent and 66 (10.7 %) were non-adherent to scheduled colonoscopy at 1 year. The relative risk for non-adherence was 5.42 [95 % confidence interval (CI) 2.74–10.75] in patients undergoing colonoscopy for screening compared to those for surveillance (16.7 vs. 3.5 % non-adherence, respectively, P  < 0.001). An indication of screening in comparison with surveillance was associated with non-adherence [odds ratio (OR) 12.69, 95 % CI 4.18–38.51] and multiple cancellations (OR 2.33, 95 % CI 1.27–4.31) by multiple regression analysis. Conclusions Patients undergoing colonoscopy for CRC screening are significantly less likely to attend their scheduled procedure within a year and have more procedure cancellations than those undergoing surveillance colonoscopy.

The objective of this study was to examine the effects of severe iron restriction on bone microarchitecture and begin to characterize the mechanism by which this occurs. Weanling Sprague Dawley rats were assigned to one of three dietary treatments for 35 days: severe iron restriction (< 3 mg Fe/kg diet), control (50 mg Fe/kg diet), or pair-fed control diet to the level of intake of the iron restricted animals. Analysis of bone mineral density (BMD) and microarchitecture were obtained by DXA and microcomputed tomography (µCT) in both the tibia and spine. RNA was extracted from the femur and used to synthesize cDNA for quantitative real-time polymerase chain reactions (qPCR). Iron deficiency was confirmed by the expression of transferrin receptor mRNA in bone marrow cells (3.6-fold higher in iron-restricted animals, p<0.05). BMD (-12%) and bone microarchitecture of spines from animals receiving both levels of iron restriction were decreased (p<0.05), whereas no changes were observed in the tibia. Trabecular number and thickness were significantly decreased (p<0.001) coupled with an increase in trabecular separation in the spine. mRNA expression analysis revealed significant down-regulation of key osteogenic factors including Runx2, osterix, and bone morphogenetic protein-2 (BMP-2). Our findings indicate that iron deficiency negatively impact the differentiation and maturation of mesenchymal stem cells into osteoblasts, based on the observed decrease in expression of BMP-2, Runx2, and osterix. Thus, our results demonstrate that severe iron deficiency during a period of rapid growth is very likely a risk factor for osteoporosis, and future research regarding the mechanism by which this occurs is warranted.