Ethanol extract of mulberry leaves partially restores the composition of intestinal microbiota and strengthens liver glycogen fragility in type 2 diabetic rats.

BACKGROUND: Mulberry leaf as a traditional Chinese medicine is able to treat obesity, diabetes, and dyslipidemia. It is well known that diabetes leads to intestinal microbiota dysbiosis. It is also recently discovered that liver glycogen structure is impaired in diabetic animals. Since mulberry leaves are able to improve the diabetic conditions through reducing blood glucose level, it would be interesting to investigate whether they have any positive effects on intestinal microbiota and liver glycogen structure. METHODS: In this study, we first determined the bioactive components of ethanol extract of mulberry leaves via high-performance liquid chromatography (HPLC) and liquid chromatography/mass spectrometry (LC/MS). Murine animal models were divided into three groups, normal Sprague-Dawley (SD) rats, high-fat diet (HFD) and streptozotocin (STZ) induced type 2 diabetic rats, and HFD/STZ-induced rats administered with ethanol extract of mulberry leaves (200 mg/kg/day). Composition of intestinal microbiota was analyzed via metagenomics by sequencing the V3-V4 region of 16S rDNAs. Liver glycogen structure was characterized through size exclusion chromatography (SEC). Both Student's t-test and Tukey's test were used for statistical analysis. RESULTS: A group of type 2 diabetic rat models were successfully established. Intestinal microbiota analysis showed that ethanol extract of mulberry leaves could partially change intestinal microbiota back to normal conditions. In addition, liver glycogen was restored from fragile state to stable state through administration of ethanol extract of mulberry leaves. CONCLUSIONS: This study confirms that the ethanol extract of mulberry leaves (MLE) ameliorates intestinal microbiota dysbiosis and strengthens liver glycogen fragility in diabetic rats. These finding can be helpful in discovering the novel therapeutic targets with the help of further investigations.

Analysis of risk factors for spontaneous rupture of hepatocellular carcinoma / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To assess the risk factors for spontaneous rupture of hepatocellular carcinoma (SRHC).</p><p><b>METHODS</b>A retrospective analysis of 34 consecutive patients with SRHC treated by emergency interventional embolization in our hospital from July 2003 to July 2011 was conducted. General condition, laboratory examination and imaging data were analyzed, and compared with the data of 34 patients with primary hepatocellular carcinoma but without rupture, randomly selected from 215 concurrent patients. The patients with SRHC were selected for risk factor analysis, and the non-SRHC patients were taken as control group.</p><p><b>RESULTS</b>No significant difference between the SRHC group and control group was found in age, sex, Child-Turcotte-Pugh (CTP) grade, Barcelona clinic liver cancer (BCLC) stage, HBsAg, HBsAb, HBeAg, HBeAb, HBcAb, prothrombin time (PT), thrombin time (TT), international normalized ratio (INR), glucose (GLU), cirrhosis, portal tumor thrombus, the maximum diameter of tumor, location, and cholecystitis or cholelithiasis. The univariate analysis showed that activated partial thromboplastin time (APTT), lower or normal plasma fibrinogen (FIB) level, alpha fetoprotein (AFP), tumor protrusion > 1 cm above the liver surface were all associated with increased risk of SRHC (P < 0.05). Multivariate analysis only showed that lower or normal level of FIB (P = 0.033) and tumor protrusion > 1 cm above the liver surface (P = 0.041) were significant independent risk factors for SRHC.</p><p><b>CONCLUSION</b>Lower or normal level of FIB and tumor protrusion > 1 cm above the liver surface are significant independent risk factors for spontaneous rupture of hepatocellular carcinoma.</p>