1.
Effects of sevelamer hydrochloride on mortality, lipid abnormality and arterial stiffness in hemodialyzed patients: a propensity-matched observational study.
Iimori, S, Mori, Y, Akita, W, Takada, S, Kuyama, T, Ohnishi, T, Shikuma, S, Ishigami, J, Tajima, M, Asai, T, et al
Clinical and experimental nephrology. 2012;(6):930-7
Abstract
BACKGROUND Cause-and-effect associations between sevelamer hydrochloride (HCl) and mortality have yet to be clarified. The effects of sevelamer HCl on mortality, lipid abnormality and arterial stiffness were examined in patients with chronic kidney disease stage 5D. METHODS The effects of sevelamer HCl were studied by a single-center cohort study that was conducted from January 1, 2005 to December 31, 2008 (n = 483). By the end of the study, 172 patients (Sevelamer group) had succeeded in continuing sevelamer HCl for >6 months (median 37 months), and 300 patients (Control group) had received calcium carbonate (n = 264) or no phosphate binder (n = 36). The mortality and other outcomes were compared between these two groups after matching by a propensity score calculated using age, gender, diabetes prevalence, and dialysis vintage. RESULTS All-cause [hazard ratio (HR) 0.4, P = 0.02] and cardiovascular (CV)-cause [HR 0.29, P = 0.03] cumulative mortality were significantly lower in the matched Sevelamer group than in the matched Control group. The matched Sevelamer group showed increased high-density lipoprotein cholesterol (P = 0.003) and no change in pulse wave velocity (PWV) and ankle-brachial index (ABI), whereas the matched Control group showed increased serum low-density lipoprotein (LDL) cholesterol (P = 0.003), increased PWV (P = 0.03), and decreased ABI (P = 0.0009). Change in serum LDL cholesterol level correlated inversely with sevelamer HCl dosage (P = 0.02). CONCLUSIONS Reduced mortality in patients with sevelamer HCl may, at least in part, be explained by an improvement in dyslipidemia and arterial stiffness by sevelamer HCl.
2.
Consumption of Bifidobacterium lactis LKM512 yogurt reduces gut mutagenicity by increasing gut polyamine contents in healthy adult subjects.
Matsumoto, M, Benno, Y
Mutation research. 2004;(2):147-53
Abstract
The possible role of probiotic metabolites on human health effects of probiotics has received little research attention. In this study, we investigated the effects of consumption of Bifidobacterium lactis LKM512-containing yogurt (LKM512 yogurt) on fecal probiotic metabolites (polyamines, lactate, and acetate) and mutagenicity in seven healthy adults (one male and six females; average age: 30.5 years). Each volunteer was provided with 100g/day of LKM512 yogurt or placebo for 2 weeks. Fecal polyamines and mutagenicity were measured by HPLC and the umu-test, respectively. Consumption of LKM512 yogurt increased fecal spermidine levels, but not fecal lactate and acetate contents. The mutagenicity level significantly reduced to 79.2% (10-91.1%) and 47.9% (0-86.8%) following consumption of LKM512 yogurt (P=0.0293) and placebo (P=0.0314), respectively. LKM512 yogurt consumption significantly reduced the mutagenicity level compared with consumption of a placebo (P=0.0489). These results suggest that increased gut spermidine level by LKM512 yogurt was responsible for the reduction of mutagenicity in the gut of healthy adults. We suggest that spermidine produced by LKM512 yogurt consumption contributes to host health as a bioantimutagenic factor; to our knowledge, these substances have not been previously reported as antimutagens from probiotics or fermented milk.
3.
Impact of LKM512 yogurt on improvement of intestinal environment of the elderly.
Matsumoto, M, Ohishi, H, Benno, Y
FEMS immunology and medical microbiology. 2001;(3):181-6
Abstract
Improvement of the intestinal environment by administration of LKM512 yogurt was examined using polyamine, haptoglobin and mutagenicity as indexes which directly reflect the health condition of the host. The concentration of spermine in feces increased significantly by 3-fold (P<0.05) at week 2 of administration of LKM512 yogurt compared with before administration, and that of putrescine, spermidine, and cadaverine also tended to increase with administration of LKM512 yogurt. The haptoglobin content in feces decreased significantly (P<0.05) at week 2 of administration of LKM512 yogurt, and it showed a negative correlation with the polyamine content, indicating that acute intestinal inflammation was suppressed. Fecal mutagenicity was measured using fecal extract and fecal precipitate. Both preparations showed similar significant decreases (P<0.05) by the administration of LKM512 yogurt, as well as a negative correlation with polyamine content. This result indicated that antimutagenicity due to administration of LKM512 yogurt was not based on binding of the mutagen to the bacterial cell wall. Many reports have suggested that polyamines increased by the administration of LKM512 yogurt led to inhibition of inflammation and antimutagenicity in the intestinal tract.