Norbert J Tripolt1, Bettina Leber2, Alexander Triebl3, Harald Köfeler4, Vanessa Stadlbauer5, Harald Sourij6. 1. Medical University of Graz, Department of Internal Medicine, Division of Endocrinology and Metabolism, Cardiovascular Diabetology Research Group, Graz, Austria. Electronic address: norbert.tripolt@medunigraz.at. 2. Medical University of Graz, Department of Internal Medicine, Division of Gastroenterology and Hepatology, Graz, Austria. Electronic address: bettina.leber@medunigraz.at. 3. Medical University of Graz, Center for Medical Research, Core Facility for Mass Spectrometry, Graz, Austria. Electronic address: alexander.triebl@medunigraz.at. 4. Medical University of Graz, Center for Medical Research, Core Facility for Mass Spectrometry, Graz, Austria. Electronic address: harald.koefeler@medunigraz.at. 5. Medical University of Graz, Department of Internal Medicine, Division of Gastroenterology and Hepatology, Graz, Austria. Electronic address: vanessa.stadlbauer@medunigraz.at. 6. Medical University of Graz, Department of Internal Medicine, Division of Endocrinology and Metabolism, Cardiovascular Diabetology Research Group, Graz, Austria; Centre for Biomarker Research in Medicine (CBmed), Graz, Austria. Electronic address: ha.sourij@medunigraz.at.
Abstract
BACKGROUND: Recent studies in animal models have shown a link between ingestion of dietary phosphatidylcholine (PC), choline, l-carnitine and cardiovascular risk. Intestinal microbiota-dependent metabolism of PC and l-carnitine is involved in formation of trimethylamine (TMA), which is further metabolized to the proatherogenic compound trimethylamine-N-oxide (TMAO). It has been suggested that changes in gut microbiota by supplementation of probiotic drinks might alter TMAO levels. Hence, the aim of this analysis was to investigate the impact of Lactobacillus casei Shirota (LcS) on formation of TMAO in subjects with metabolic syndrome. METHODS: In a single-center, prospective, randomized-controlled study 30 subjects with metabolic syndrome were randomized to receive either 3 times daily 6.5 × 10(9) CFU (colony-forming units) LcS (probiotic group) or not (standard therapy group) for 12 weeks. TMAO plasma levels were quantified by means of liquid chromatography and tandem mass spectrometry. RESULTS:Thirteen patients in the probiotic group and 15 in the standard therapy group finished the study. Mean age was 52 ± 11 and 55 ± 9 years, respectively. TMAO levels decreased during the intervention period in both groups (from 4.66 ± 2.66 μM to 4.31 ± 2.04 μM in the probiotic group and from 4.64 ± 2.75 μM to 4.40 ± 2.14 μM in the control group). Changes in TMAO between subjects receiving LcS (-0.25 ± 2.39 μM) and controls (-0.34 ± 2.23 μM) were not significantly different (p = 0.510). CONCLUSION: In conclusion, intake of LcS for 12 weeks did not affect levels of TMAO in patients with metabolic syndrome.
RCT Entities:
BACKGROUND: Recent studies in animal models have shown a link between ingestion of dietary phosphatidylcholine (PC), choline, l-carnitine and cardiovascular risk. Intestinal microbiota-dependent metabolism of PC and l-carnitine is involved in formation of trimethylamine (TMA), which is further metabolized to the proatherogenic compound trimethylamine-N-oxide (TMAO). It has been suggested that changes in gut microbiota by supplementation of probiotic drinks might alter TMAO levels. Hence, the aim of this analysis was to investigate the impact of Lactobacillus casei Shirota (LcS) on formation of TMAO in subjects with metabolic syndrome. METHODS: In a single-center, prospective, randomized-controlled study 30 subjects with metabolic syndrome were randomized to receive either 3 times daily 6.5 × 10(9) CFU (colony-forming units) LcS (probiotic group) or not (standard therapy group) for 12 weeks. TMAO plasma levels were quantified by means of liquid chromatography and tandem mass spectrometry. RESULTS: Thirteen patients in the probiotic group and 15 in the standard therapy group finished the study. Mean age was 52 ± 11 and 55 ± 9 years, respectively. TMAO levels decreased during the intervention period in both groups (from 4.66 ± 2.66 μM to 4.31 ± 2.04 μM in the probiotic group and from 4.64 ± 2.75 μM to 4.40 ± 2.14 μM in the control group). Changes in TMAO between subjects receiving LcS (-0.25 ± 2.39 μM) and controls (-0.34 ± 2.23 μM) were not significantly different (p = 0.510). CONCLUSION: In conclusion, intake of LcS for 12 weeks did not affect levels of TMAO in patients with metabolic syndrome.
Authors: Nora A Kalagi; Kylie A Abbott; Khalid A Alburikan; Hadeel A Alkofide; Elizabeth Stojanovski; Manohar L Garg Journal: Adv Nutr Date: 2019-09-01 Impact factor: 8.701
Authors: Tanya T Nguyen; Tomasz Kosciolek; Rebecca E Daly; Yoshiki Vázquez-Baeza; Austin Swafford; Rob Knight; Dilip V Jeste Journal: Brain Behav Immun Date: 2020-10-22 Impact factor: 7.217