BackgroundGrowing evidence indicates that intestinal microbiota regulate our metabolism. Probiotics confer health benefits that may depend on their ability to affect the gut microbiota. The objective of this study was to examine the effect of supplementation with the probiotic strain, Lactobacillus rhamnosus hsryfm 1301, on the gut microbiota in a hyperlipidemic rat model, and to explore the associations between the gut microbiota and the serum lipids.MethodsThe hyperlipidemic rat model was established by feeding rats a high-fat diet for 28 d. The rats’ gut microbiota were analyzed using high-throughput sequencing before and after L. rhamnosus hsryfm 1301 supplementation or its fermented milk for 28 d. The serum lipids level was also tested.ResultsThe rats’ primary gut microbiota were composed of Bacteroidetes, Firmicutes, Proteobacteria, Spirochaetes and Verrucomicrobia. The abundance and diversity of the gut microbiota generally decreased after feeding with a high-fat diet, with a significant decrease in the relative abundance of Bacteroidetes, but with an increase in that of Firmicutes (P < 0.05). Administration of L. rhamnosus hsryfm 1301 or its fermented milk for 28 d, could recover the Bacteroidetes and Verrucomicrobia abundance and could decrease the Firmicutes abundance, which was associated with a significant reduction in the serum lipids’ level in the hyperlipidemic rats with high-fat diet induced. The abundance of 22 genera of gut bacteria was changed significantly after probiotic intervention for 28 d (P < 0.05). A positive correlation was observed between Ruminococcus spp. and serum triglycerides, Dorea spp. and serum cholesterol (TC) and low-density lipoprotein (LDL-C), and Enterococcus spp. and high-density lipoprotein. The Butyrivibrio spp. negatively correlated with TC and LDL-C.ConclusionsOur results suggest that the lipid metabolism of hyperlipidemic rats was improved by regulating the gut microbiota with supplementation of L.rhamnosus hsryfm 1301 or its fermented milk for 28 d.Electronic supplementary materialThe online version of this article (doi:10.1186/1472-6882-14-386) contains supplementary material, which is available to authorized users.

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BackgroundPostural tachycardia syndrome (POTS) is a heterogeneous disorder that creates challenges for treatment. Beta-blocker was one of the most commonly used drugs, but it is inconsistently effective. The purpose of this study is to explore whether orthostatic plasma norepinephrine level could be an indicator of therapeutic effectiveness of metoprolol for POTS in children.MethodsTwenty-seven children with POTS were enrolled in our study. They received metoprolol treatment, and their orthostatic plasma norepinephrine levels were measured by high-performance liquid chromatography method. Three months after rmetoprolol treatment, 25 patients were followed up. A receiver-operating characteristic (ROC) curve was used to explore the predictive value of orthostatic plasma norepinephrine level.ResultsThe symptom severity and increment of heat rate from supine position to upright of patients positively correlated with their orthostatic plasma norepinephrine level (r = 0.599, P < 0.001; r = 0.633, P <0.001, respectively). Orthostatic plasma norepinephrine level in responders to metoprolol was significantly higher than that of nonresponders (P = 0.028). A ROC curve on the predictive value of orthostatic plasma norepinephrine level showed that the area under the curve was 0.785. Using a cutoff value for orthostatic plasma norepinephrine level of 3.59 pg/ml yielded both sensitivity (76.9%) and specificity (91.7%) in predicting the efficacy of metoprolol therapy for POTS.ConclusionOrthostatic plasma norepinephrine level of > 3.59 pg/ml was an indicator of the effectiveness of metoprolol therapy for POTS in children and adolescents.

Corilagin (Cori) possesses multiple biological activities. To determine whether Cori can exert protective effects against nonalcoholic fatty liver disease (NAFLD) and its potential mechanisms. C57BL/6 mice were fed with high-fat diet (HFD) alone or in combination with Cori (20 mg/kg, i.p.) and AML12 cells were exposed to 200 mM PA/OA with or without Cori (10 mM or 20 mM). Phenotypes and key indicators relevant to NAFLD were examined both in vivo and in vitro. In this study, Cori significantly ameliorated hepatic steatosis, confirmed by improved serum lipid profiles, and hepatic TC, TG contents, and the gene expression related to lipid metabolism in livers of HFD mice. Moreover, Cori attenuated HFD-mediated autophagy (including mitophagy) blockage by restoring autophagic flux, evidenced by increased number of autophagic double vesicles containing mitochondria, elevated LC3II protein levels, decreased p62 protein levels, as well as enhanced colocalization of autophagy-related protein (LC3, Parkin) and mitochondria. In accordance with this, Cori also reduced the accumulation of ROS and MDA levels, and enhanced the activities of antioxidative enzymes including SOD, GSH-Px, and CAT. In addition, Cori treatment improved mitochondrial dysfunction, evidenced by increased mitochondrial membrane potential (DYm). In parallel with this, Cori decreased mitochondrial DNA oxidative damage, while increased mitochondrial biogenesis related transcription factors expression, mitochondrial DNA content and oxygen consumption rate (OCR). In conclusion, these results demonstrate that Cori is a potential candidate for

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