Resistance of Amphiphilic Polysaccharides against Marine Fouling Organisms.

Amphiphilic coatings are promising candidates for fouling-release applications. As hydrophilic components, polysaccharides are interesting and environmentally benign building blocks. We used covalently coupled alginic acid (AA) and hyaluronic acid (HA) and postmodified them with a hydrophobic fluorinated amine. The surfaces showed good stability under marine conditions and fluorination led to a decreased uptake of Ca(2+) ions after modification. In single species settlement assays (bacteria, diatoms, barnacle cypris larvae), the modification decreased the settlement density and/or the adhesion strength of many of the tested species. Field studies supported findings of the laboratory experiments, as hydrophobic modification of AA and HA decreased diatom colonization.

Infant formula containing galacto-and fructo-oligosaccharides and Bifidobacterium breve M-16V supports adequate growth and tolerance in healthy infants in a randomised, controlled, double-blind, prospective, multicentre study.

The objective of the present study was to evaluate the growth and tolerance in healthy, term infants consuming a synbiotic formula with daily weight gain as the primary outcome. In a randomised, controlled, double-blind, multicentre, intervention study infants were assigned to an extensively hydrolysed formula containing a specific combination of Bifidobacterium breve M-16V and a prebiotic mixture (short-chain galacto-oligosaccharides and long-chain fructo-oligosaccharides in a 9:1 ratio; scGOS/lcFOS; synbiotic group), or the same formula without this synbiotic concept for 13 weeks (control group). Anthropometry, formula intake, tolerance, stool characteristics, blood parameters, faecal microbiota and metabolic faecal profile were assessed. Medically confirmed adverse events were recorded throughout the study. Equivalence in daily weight gain was demonstrated for the intention-to-treat (ITT) population (n 211). In the per-protocol (PP) population (n 102), the 90 % CI of the difference in daily weight gain slightly crossed the lower equivalence margin. During the intervention period, the mean weight-for-age and length-for-age values were close to the median of the WHO growth standards in both groups, indicating adequate growth. The number of adverse events was not different between both groups. No relevant differences were observed in blood parameters indicative for liver and renal function. At 13 weeks, an increased percentage of faecal bifidobacteria (60 v. 48 %) and a reduced percentage of Clostridium lituseburense/C. histolyticum (0·2 v. 2·6 %) were observed in the synbiotic group (n 19) compared with the control group (n 27). In conclusion, this study demonstrates that an extensively hydrolysed formula with B. breve M-16V and the prebiotic mixture scGOS/lcFOS (9:1) supports an adequate infant growth.

Microfluidic detachment assay to probe the adhesion strength of diatoms.

Fouling release (FR) coatings are increasingly applied as an environmentally benign alternative for controlling marine biofouling. As the technology relies on removing fouling by water currents created by the motion of ships, weakening of adhesion of adherent organisms is the key design goal for improved coatings. In this paper, a microfluidic shear force assay is used to quantify how easily diatoms can be removed from surfaces. The experimental setup and the optimization of the experimental parameters to study the adhesion of the diatom Navicula perminuta are described. As examples of how varying the physico-chemical surface properties affects the ability of diatoms to bind to surfaces, a range of hydrophilic and hydrophobic self-assembled monolayers was compared. While the number of cells that attached (adhered) was barely affected by the coatings, the critical shear stress required for their removal from the surface varied significantly.

Conditioning of self-assembled monolayers at two static immersion test sites along the east coast of Florida and its effect on early fouling development.

Among the first events after immersion of surfaces in the ocean is surface 'conditioning'. Here, the accumulation and composition of the conditioning films formed after immersion in the ocean are analyzed. In order to account for different surface chemistries, five self-assembled monolayers that differ in resistance to microfouling and wettability were used. Water samples from two static immersion test sites along the east coast of Florida were collected at two different times of the year and used for experiments. Spectral ellipsometry revealed that conditioning films were formed within the first 24 h and contact angle goniometry showed that these films changed the wettability and rendered hydrophobic surfaces more hydrophilic and vice versa. Infrared reflection adsorption spectroscopy showed that the composition of the conditioning film depended on both the wettability and immersion site. Laboratory and field assays showed that the presence of a conditioning film did not markedly influence settlement of microorganisms.

Feasibility and effectiveness of an evidence-based asthma service in Australian community pharmacies: a pragmatic cluster randomized trial.

OBJECTIVE: To test the feasibility, effectiveness, and sustainability of a pharmacy asthma service in primary care. METHODS: A pragmatic cluster randomized trial in community pharmacies in four Australian states/territories in 2009. Specially trained pharmacists were randomized to deliver an asthma service in two groups, providing three versus four consultations over 6 months. People with poorly controlled asthma or no recent asthma review were included. Follow-up for 12 months after service completion occurred in 30% of randomly selected completing patients. Outcomes included change in asthma control (poor and fair/good) and Asthma Control Questionnaire (ACQ) score, inhaler technique, quality of life, perceived control, adherence, asthma knowledge, and asthma action plan ownership. RESULTS: Ninety-six pharmacists enrolled 570 patients, with 398 (70%) completing. Asthma control significantly improved with both the three- and four-visit service, with no significant difference between groups (good/fair control 29% and 21% at baseline, 61% and 59% at end, p = .791). Significant improvements were also evident in the ACQ (mean change 0.56), inhaler technique (17-33% correct baseline, 57-72% end), asthma action plan ownership (19% baseline, 56% end), quality of life, adherence, perceived control, and asthma knowledge, with no significant difference between groups for any variable. Outcomes were sustained at 12 months post-service. CONCLUSIONS: The pharmacy asthma service delivered clinically important improvements in both a three-visit and four-visit service. Pharmacists were able to recruit and deliver the service with minimal intervention, suggesting it is practical to implement in practice. The three-visit service would be feasible and effective to implement, with a review at 12 months.

The role and requirements of digestible dietary carbohydrates in infants and toddlers.

Digestible carbohydrates are one of the main sources of dietary energy in infancy and childhood and are essential for growth and development. The aim of this narrative review is to outline the intakes of digestible carbohydrates and their role in health and disease, including the development of food preferences, as well the consequences of excess carbohydrate. Key experts in these fields provided up-to-date reviews of the literature. A search of available information on dietary intakes of children below the age of 4 years was conducted from 1985 up to 2010. Articles and reports including information about sugars and/or starch intakes were selected. A number of factors limit the ability to obtain an overall picture of carbohydrate intakes and food sources in this age group. These include small numbers of intake studies, differing approaches to analysing carbohydrate, a variety of terms used to describe sugars intakes and a dearth of information about starch intakes. Data suggest that sweet taste is preferred in infancy and later food choices. There are few established adverse consequences of high intakes of digestible carbohydrate for young children. The greatest evidence is for dental caries, although this is influenced by high intake frequency and poor oral hygiene. Evidence for detrimental effects on nutrient dilution, obesity, diabetes or cognition is limited. In infants, minimum carbohydrate (mainly lactose) intake should be 40% of total energy, gradually increasing to 55% energy by the age of 2 years.

ELF5 suppresses estrogen sensitivity and underpins the acquisition of antiestrogen resistance in luminal breast cancer.

We have previously shown that during pregnancy the E-twenty-six (ETS) transcription factor ELF5 directs the differentiation of mammary progenitor cells toward the estrogen receptor (ER)-negative and milk producing cell lineage, raising the possibility that ELF5 may suppress the estrogen sensitivity of breast cancers. To test this we constructed inducible models of ELF5 expression in ER positive luminal breast cancer cells and interrogated them using transcript profiling and chromatin immunoprecipitation of DNA followed by DNA sequencing (ChIP-Seq). ELF5 suppressed ER and FOXA1 expression and broadly suppressed ER-driven patterns of gene expression including sets of genes distinguishing the luminal molecular subtype. Direct transcriptional targets of ELF5, which included FOXA1, EGFR, and MYC, accurately classified a large cohort of breast cancers into their intrinsic molecular subtypes, predicted ER status with high precision, and defined groups with differential prognosis. Knockdown of ELF5 in basal breast cancer cell lines suppressed basal patterns of gene expression and produced a shift in molecular subtype toward the claudin-low and normal-like groups. Luminal breast cancer cells that acquired resistance to the antiestrogen Tamoxifen showed greatly elevated levels of ELF5 and its transcriptional signature, and became dependent on ELF5 for proliferation, compared to the parental cells. Thus ELF5 provides a key transcriptional determinant of breast cancer molecular subtype by suppression of estrogen sensitivity in luminal breast cancer cells and promotion of basal characteristics in basal breast cancer cells, an action that may be utilised to acquire antiestrogen resistance.

The antiproliferative effects of progestins in T47D breast cancer cells are tempered by progestin induction of the ETS transcription factor Elf5.

Prolactin and progesterone act together to regulate mammary alveolar development, and both hormones have been implicated in breast cancer initiation and progression. Here we show that Elf5, a prolactin-induced ETS transcription factor that specifies the mammary secretory cell lineage, is also induced by progestins in breast cancer cells via a direct mechanism. To define the transcriptional response to progestin elicited via Elf5, we made an inducible Elf5 short hairpin-RNA knock-down model in T47D breast cancer cells and used it to prevent the progestin-induction of Elf5. Functional analysis of Affymetrix gene expression data using Gene Ontologies and Gene Set Enrichment Analysis showed enhancement of the progestin effects on cell cycle gene expression. Cell proliferation assays showed a more efficacious progestin-induced growth arrest when Elf5 was kept at baseline levels. These results showed that progestin induction of Elf5 expression tempered the antiproliferative effects of progestins in T47D cells, providing a further mechanistic link between prolactin and progestin in the regulation of mammary cell phenotype.

Meta-analysis and gene set enrichment relative to er status reveal elevated activity of MYC and E2F in the "basal" breast cancer subgroup.

BACKGROUND: Breast cancers lacking the estrogen receptor (ER) can be distinguished from other breast cancers on the basis of poor prognosis, high grade, distinctive histopathology and unique molecular signatures. These features further distinguish estrogen receptor negative (ER-) tumor subtypes, but targeted therapy is currently limited to tumors over-expressing the ErbB2 receptor. METHODOLOGY/PRINCIPAL FINDINGS: To uncover the pathways against which future therapies could be developed we undertook a meta-analysis of gene expression from five large microarray datasets relative to ER status. A measure of association with ER status was calculated for every Affymetrix HG-U133A probe set and the pathways that distinguished ER- tumors were defined by testing for enrichment of biologically defined gene sets using Gene Set Enrichment Analysis (GSEA). As expected, the expression of the direct transcriptional targets of the ER was muted in ER- tumors, but the expression of genes indirectly regulated by estrogen was enhanced. We also observed enrichment of independent MYC- and E2F-driven transcriptional programs. We used a cell model of estrogen and MYC action to define the interaction between estrogen and MYC transcriptional activity in breast cancer. We found that the basal subgroup of ER- breast cancer showed a strong MYC transcriptional response that reproduced the indirect estrogen response seen in estrogen receptor positive (ER+) breast cancer cells. CONCLUSIONS/SIGNIFICANCE: Increased transcriptional activity of MYC is a characteristic of basal breast cancers where it mimics a large part of an estrogen response in the absence of the ER, suggesting a mechanism by which these cancers achieve estrogen-independence and providing a potential therapeutic target for this poor prognosis sub group of breast cancer.

HSD17B4 overexpression, an independent biomarker of poor patient outcome in prostate cancer.

Steroid hormones and their metabolising enzymes have been studied extensively for their potential role in prostate cancer, with more recent interest in the androgen/estrogen inactivating enzyme 17beta-hydroxysteroid dehydrogenase type 4 (HSD17B4). Gene expression profiling showed HSD17B4 to be significantly overexpressed in prostate cancer compared to matched-benign epithelium. We therefore hypothesized that altered HSD17B4 expression may contribute to prostate cancer progression via altered hormone balance. In this study, HSD17B4 mRNA and protein expression were assessed by in situ hybridisation (ISH) and immunohistochemistry (IHC), respectively, in tissue arrays of prostate tissue from 172 patients treated by radical prostatectomy. Overexpression of HSD17B4 mRNA and protein was associated with prostate cancer (P<0.0001) and multivariate Cox proportional hazards analysis, adjusted for known prognostic indicators, demonstrated HSD17B4 mRNA and high protein expression were significant independent predictors of poor patient outcome as measured by time until PSA relapse (mRNA: hazards ratio [HR]=1.90, 95% confidence interval [CI]=1.15-3.12; P<0.0001; and protein: HR=2.09, 95% CI=1.31-3.33; P=0.0026). Here we provide strong evidence that both mRNA and protein overexpression of HSD17B4 is not only associated with the presence of prostate cancer, but is also a significant independent predictor of poor patient outcome.

Identification of functional networks of estrogen- and c-Myc-responsive genes and their relationship to response to tamoxifen therapy in breast cancer.

BACKGROUND: Estrogen is a pivotal regulator of cell proliferation in the normal breast and breast cancer. Endocrine therapies targeting the estrogen receptor are effective in breast cancer, but their success is limited by intrinsic and acquired resistance. METHODOLOGY/PRINCIPAL FINDINGS: With the goal of gaining mechanistic insights into estrogen action and endocrine resistance, we classified estrogen-regulated genes by function, and determined the relationship between functionally-related genesets and the response to tamoxifen in breast cancer patients. Estrogen-responsive genes were identified by transcript profiling of MCF-7 breast cancer cells. Pathway analysis based on functional annotation of these estrogen-regulated genes identified gene signatures with known or predicted roles in cell cycle control, cell growth (i.e. ribosome biogenesis and protein synthesis), cell death/survival signaling and transcriptional regulation. Since inducible expression of c-Myc in antiestrogen-arrested cells can recapitulate many of the effects of estrogen on molecular endpoints related to cell cycle progression, the estrogen-regulated genes that were also targets of c-Myc were identified using cells inducibly expressing c-Myc. Selected genes classified as estrogen and c-Myc targets displayed similar levels of regulation by estrogen and c-Myc and were not estrogen-regulated in the presence of siMyc. Genes regulated by c-Myc accounted for 50% of all acutely estrogen-regulated genes but comprised 85% (110/129 genes) in the cell growth signature. siRNA-mediated inhibition of c-Myc induction impaired estrogen regulation of ribosome biogenesis and protein synthesis, consistent with the prediction that estrogen regulates cell growth principally via c-Myc. The 'cell cycle', 'cell growth' and 'cell death' gene signatures each identified patients with an attenuated response in a cohort of 246 tamoxifen-treated patients. In multivariate analysis the cell death signature was predictive independent of the cell cycle and cell growth signatures. CONCLUSIONS/SIGNIFICANCE: These functionally-based gene signatures can stratify patients treated with tamoxifen into groups with differing outcome, and potentially identify distinct mechanisms of tamoxifen resistance.

Identification of downstream targets of estrogen and c-myc in breast cancer cells.

Estrogen (E) plays a pivotal regulatory role in the control of cell proliferation in the normal breast and breast cancer (BC). To identify genes with likely roles in proliferation control that are regulated by E and its downstream target c-myc, we compared transcript profiles of antiestrogens-arrested cells stimulated to reinitiate cell cycle progression by E treatment or c-myc induction. Approximately 2/3 of the probe sets significantly regulated by E (adjusted p < 0.01) increased in expression. Half of the E-regulated probe sets were also regulated by c-myc. Genes involved in cell growth, cell proliferation, and cell survival were over-represented in the E-regulated geneset. Analysis of selected candidates has identified a nucleolar protein whose expression is correlated with c-myc expression in BC cell lines. These data indicate that a significant component of E-induced mitogenesis is mediated by c-myc and that selected c-myc target genes may be surrogate markers of c-myc expression in BC.

c-Myc overexpression and endocrine resistance in breast cancer.

The oncoprotein c-Myc is frequently overexpressed in breast cancer and ectopic expression in breast cancer cell lines attenuates responses to antiestrogen treatment. Here, we review preliminary data aimed at further elucidating a potential role for c-Myc in clinical endocrine resistance in breast cancer. Immunohistochemical and semi-quantitative PCR revealed that c-Myc protein and c-myc mRNA were frequently overexpressed in both ER-positive and ER-negative breast carcinoma. Furthermore, both constitutive and inducible c-Myc overexpression in MCF-7 breast cancer cell lines markedly reduced their sensitivity to the growth inhibitory effects of the pure antiestrogen ICI 182,780. In order to identify potential downstream targets of c-Myc that mediate this effect, Affymetrix microarrays were employed to examine the patterns of gene expression shared by MCF-7 cells stimulated by estrogen, or by induction of c-Myc. Approximately 50% of estrogen target genes identified 6h after treatment were also regulated by c-Myc. One novel target, EMU4, was transcriptionally regulated by c-Myc. In addition, there was a strong correlation between c-myc and EMU4 mRNA expression in a battery of breast cancer cell lines. These data confirm that c-Myc overexpression is a common event in breast cancer, and that this is associated with resistance to antiestrogens in vitro. Furthermore, the development of an experimental paradigm for the discovery of c-Myc and estrogen target genes associated with endocrine resistance provides a framework for the discovery and validation of genes involved in estrogen signalling, and c-Myc-mediated-antiestrogen resistance.

Intratympanic steroid therapy for inner ear diseases, a review of the literature.

To evaluate the value of clinical trials on intratympanic steroid therapy in Ménière's disease (MD), idiopathic sudden sensorineural hearing loss (ISSNHL) and rapidly progressive sensorineural hearing loss (RPSNHL). Medline and Pubmed databases from 1966 to present were searched for clinical studies on intra- or transtympanic (cortico)steroid therapy of MD, ISSNHL and RPSNHL. Results were cross-checked with additional databases to obtain a complete data set. Clinical trials were evaluated on the basis of comparability, internal and external validity. Articles were judged using the following questions: was a randomised double-blind controlled trial performed? Which criteria were used to confirm the diagnosis of MD, ISSNHL, RPSNHL? Which therapy was evaluated? How long was the follow-up? Which criteria were used to evaluate the results? Reliable evidence on the efficiency, optimum dosage and administration schedule of intratympanic steroid therapy in MD, ISSNHL and RPSNHL is lacking, therefore further investigation is required.

Faecal SIgA secretion in infants fed on pre- or probiotic infant formula.

Secretory immunoglobulin A (SIgA) plays an important role in the defence of the gastrointestinal tract. The level of faecal SIgA antibody is associated with increased neutralization and clearance of viruses. Formula-fed infants who lack the transfer of protective maternal SIgA from breast milk may benefit from strategies to support maturation of humoral immunity and endogenous production of SIgA. We aimed at studying the effects of standard, prebiotic and probiotic infant formulas on the faecal SIgA levels. At birth, infants of whom the mother had decided not to breastfeed were allocated to one of three formula groups in a randomized, double-blind fashion. Nineteen infants received standard infant formula; 19 received prebiotic formula containing a specific mixture of 0.6 g galacto-oligosaccharides (GOS)/fructo-oligosaccharides (FOS)/100 ml formula and 19 received probiotic formula containing 6.0 x 10(9) cfu Bifidobacterium animalis/100 ml formula. Faecal samples were taken on postnatal day 5, day 10, wk 4 and every 4 wk thereafter until wk 32. SIgA in faeces was determined by an enzyme-linked immunosorbent assay. During the intervention, infants fed on prebiotic formula showed a trend towards higher faecal SIgA levels compared with the standard formula-fed infants reaching statistical significance at the age of 16 wk. In contrast, infants fed on the probiotic formula showed a highly variable faecal SIgA concentration with no statistically significant differences compared with the standard formula group. Formula-fed infants may benefit from infant formulas containing a prebiotic mixture of GOS and FOS because of the observed clear tendency to increase faecal SIgA secretion. Adding viable B. animalis strain Bb-12 to infant formula did not reveal any sign for such a trend.

Molecular evolutionary relationships of enteroinvasive Escherichia coli and Shigella spp.

Enteroinvasive Escherichia coli (EIEC), a distinctive pathogenic form of E. coli causing dysentery, is similar in many properties to bacteria placed in the four species of Shigella. Shigella has been separated as a genus but in fact comprises several clones of E. coli. The evolutionary relationships of 32 EIEC strains of 12 serotypes have been determined by sequencing of four housekeeping genes and two plasmid genes which were used previously to determine the relationships of Shigella strains. The EIEC strains were grouped in four clusters with one outlier strain, indicating independent derivation of EIEC several times. Three of the four clusters contain more than one O antigen type. One EIEC strain (an O112ac:H- strain) was found in Shigella cluster 3 but is not identical to the Shigella cluster 3 D2 and B15 strains with the same O antigen. Two forms of the virulence plasmid pINV have been identified in Shigella strains by using the sequences of ipgD and mxiA genes, and all but two of our EIEC strains have pINV A. The EIEC strains were grouped in two subclusters with a very low level of variation, generally not intermingled with Shigella pINV A strains. The EIEC clusters based on housekeeping genes were reflected in the plasmid gene sequences, with some exceptions. Two strains were found in the pINV B form by using the ipgD sequence, with one strain having an mxiA sequence similar to the divergent sequence of D1. Clearly, EIEC and Shigella spp. form a pathovar of E. coli.

The bovine protein alpha-lactalbumin increases the plasma ratio of tryptophan to the other large neutral amino acids, and in vulnerable subjects raises brain serotonin activity, reduces cortisol concentration, and improves mood under stress.

BACKGROUND: Increased brain serotonin may improve the ability to cope with stress, whereas a decline in serotonin activity is involved in depressive mood. The uptake of the serotonin precursor, tryptophan, into the brain is dependent on nutrients that influence the cerebral availability of tryptophan via a change in the ratio of plasma tryptophan to the sum of the other large neutral amino acids (Trp-LNAA ratio). Therefore, a diet-induced increase in tryptophan availability may increase brain serotonin synthesis and improve coping and mood, particularly in stress-vulnerable subjects. OBJECTIVE: We tested whether alpha-lactalbumin, a whey protein with a high tryptophan content, may increase the plasma Trp-LNAA ratio and reduce depressive mood and cortisol concentrations in stress-vulnerable subjects under acute stress. DESIGN: Twenty-nine highly stress-vulnerable subjects and 29 relatively stress-invulnerable subjects participated in a double-blind, placebo-controlled study. Subjects were exposed to experimental stress after the intake of a diet enriched with either alpha-lactalbumin or sodium-caseinate. Diet-induced changes in the plasma Trp-LNAA ratio and prolactin were measured. Changes in mood, pulse rate, skin conductance, and cortisol concentrations were assessed before and after the stressor. RESULTS: The plasma Trp-LNAA ratio was 48% higher after the alpha-lactalbumin diet than after the casein diet (P = 0.0001). In stress-vulnerable subjects this was accompanied by higher prolactin concentrations (P = 0.001), a decrease in cortisol (P = 0.036), and reduced depressive feelings (P = 0.007) under stress. CONCLUSIONS: Consumption of a dietary protein enriched in tryptophan increased the plasma Trp-LNAA ratio and, in stress-vulnerable subjects, improved coping ability, probably through alterations in brain serotonin.

Effect of transgalactooligosaccharides on the composition of the human intestinal microflora and on putative risk markers for colon cancer.

BACKGROUND: Nondigestible oligosaccharides have been claimed to benefit the health of the colon by selectively stimulating the growth of bifidobacteria and by decreasing the toxicity of the colon contents. OBJECTIVE: We compared the effect of 2 doses of transgalactooligosaccharides and a placebo on the composition and activity of the intestinal microflora in 18 women and 22 men. DESIGN: Strictly controlled experimental diets were supplied to 3 intervention groups in a parallel design. The study was divided into 2 consecutive 3-wk periods during which each participant consumed a run-in diet followed by an intervention diet that differed only in the amount of transgalactooligosaccharides: 0 (placebo), 7.5, and 15 g/d. Breath samples and fecal samples were collected at the end of both the run-in and intervention periods. RESULTS: Apparent fermentability of transgalactooligosaccharides was 100%. The highest dose of transgalactooligosaccharides significantly increased the concentration of breath hydrogen by 130% (P < 0.01) and the nitrogen density of the feces by 8.5% (P < 0.05). The number of bifidobacteria increased after both placebo and transgalactooligosaccharides ingestion, but the differences between these increases were not significantly different. Transgalactooligosaccharides did not significantly affect bowel habits; stool composition; the concentration of short-chain fatty acids or bile acids in fecal water; the concentration of ammonia, indoles, or skatoles in feces; fecal pH; or the composition of the intestinal microflora. CONCLUSION: We conclude that transgalactooligosaccharides are completely fermented in the human colon, but do not beneficially change the composition of the intestinal microflora, the amount of protein fermentation products in feces, or the profile of bile acids in fecal water.

Consumption of fructooligosaccharides does not favorably affect blood glucose and serum lipid concentrations in patients with type 2 diabetes.

BACKGROUND: Fructooligosaccharides have been claimed to lower fasting glycemia and serum total cholesterol concentrations, possibly via effects of short-chain fatty acids produced during fermentation. OBJECTIVE: We studied the effects of fructooligosaccharides on blood glucose, serum lipids, and serum acetate in 20 patients with type 2 diabetes. DESIGN: In a randomized, single-blind, crossover design, patients consumed either glucose as a placebo (4 g/d) or fructooligosaccharides (15 g/d) for 20 d each. Average daily intakes of energy, macronutrients, and dietary fiber were similar with both treatments. RESULTS: Compliance, expressed as the proportion of supplements not returned, was near 100% during both treatments. Fructooligosaccharides did not significantly affect fasting concentrations (mmol/L) of serum total cholesterol (95% CI: -0.07, 0.48), HDL cholesterol (-0.04, 0.04), LDL cholesterol (-0.06, 0.34), serum triacylglycerols (-0.21, 0.44), serum free fatty acids (-0.08, 0.04), serum acetate (-0.01, 0.01), or blood glucose (-0.37, 0.40). CONCLUSIONS: We conclude that 20 d of dietary supplementation with fructooligosaccharides had no major effect on blood glucose, serum lipids, or serum acetate in patients with type 2 diabetes. This lack of effect was not due to changes in dietary intake, insufficient statistical power, or noncompliance of the patients.

Bacterial fermentation of fructooligosaccharides and resistant starch in patients with an ileal pouch-anal anastomosis.

Patients with large bowel disease may undergo ileal pouch-anal anastomosis, in which the colon is removed and part of the distal ileum is used to construct a pelvic reservoir. Competence of the ileal pouch to ferment carbohydrates is associated with the absence of pouchitis. However, the extent to which bacterial fermentation takes place and whether it is affected by diet are unclear. We investigated fermentation of two nondigestible carbohydrates, fructooligosaccharides and resistant starch, in 15 healthy patients with an ileal pouch by using a placebo-controlled crossover design (with glucose as the placebo). Apparent fermentability of fructooligosaccharides was 83%; that of resistant starch was 46%. Resistant starch increased fecal excretion of butyrate by 69% whereas fructooligosaccharides reduced excretion of amino acid-derived isobutyrate by 94% and of isovalerate by 77%. Fructooligosaccharides also significantly increased fecal weight (651 compared with 541 g/d) and breath-hydrogen excretion (286 compared with 85 ppm x h). Bacterial fermentation of nondigestible carbohydrates in pouches takes place to an appreciable extent and in a substrate-specific manner. The relation between such fermentation and inflammation of the pouch (pouchitis) deserves study.