Antiobesity and lipid-lowering effects of Bifidobacterium spp. in high fat diet-induced obese rats

<p>Abstract</p> <p>Background</p> <p>Recent studies have reported the preventive effects of probiotics on obesity. Among commensal bacteria, bifidobacteria is one of the most numerous probiotics in the mammalian gut and are a type of lactic acid bacteria. The aim of this study was to assess the antiobesity and lipid-lowering effects of <it>Bifidobacterium </it>spp. isolated from healthy Korean on high fat diet-induced obese rats.</p> <p>Methods</p> <p>Thirty-six male Sprague-Dawley rats were divided into three groups as follows: (1) SD group, fed standard diet; (2) HFD group, fed high fat diet; and (3) HFD-LAB group, fed high fat diet supplemented with LAB supplement (<it>B. pseudocatenulatum </it>SPM 1204, <it>B. longum </it>SPM 1205, and <it>B. longum </it>SPM 1207; 10⁸~ 10⁹CFU). After 7 weeks, the body, organ, and fat weights, food intake, blood serum levels, fecal LAB counts, and harmful enzyme activities were measured.</p> <p>Results</p> <p>Administration of LAB reduced body and fat weights, blood serum levels (TC, HDL-C, LDL-C, triglyceride, glucose, leptin, AST, ALT, and lipase levels), and harmful enzyme activities (β-glucosidase, β-glucuronidase, and tryptophanase), and significantly increased fecal LAB counts.</p> <p>Conclusion</p> <p>These data suggest that <it>Bifidobacterium </it>spp. used in this study may have beneficial antiobesity effects.</p

Genetic Variations Mir-10Aa\u3eT, Mir-30Ca\u3eG, Mir-181At\u3eC, and Mir-499Ba\u3eG and the Risk of Recurrent Pregnancy Loss in Korean Women

This study investigated the genetic association between recurrent pregnancy loss (RPL) and microRNA (miRNA) polymorphisms in miR-10aA\u3eT, miR-30cA\u3eG, miR-181aT\u3eC, and miR-499bA\u3eG in Korean women. Blood samples were collected from 381 RPL patients and 281 control participants, and genotyping of miR-10aA\u3eT, miR-30cA\u3eG, miR-181aT\u3eC, and miR-499bA\u3eG was carried out by TaqMan miRNA RT-Real Time polymerase chain reaction (PCR). Four polymorphisms were identified, including miR-10aA\u3eT, miR-30cA\u3eG, miR-181aT\u3eC, and miR-499bA\u3eG. MiR-10a dominant model (AA vs. AT + TT) and miR-499bGG genotypes were associated with increased RPL risk (adjusted odds ratio [AOR] = 1.520, 95% confidence interval [CI] = 1.038−2.227, p = 0.032; AOR = 2.956, 95% CI = 1.168−7.482, p = 0.022, respectively). Additionally, both miR-499 dominant (AA vs. AG + GG) and recessive (AA + AG vs. GG) models were significantly associated with increased RPL risk (AOR = 1.465, 95% CI = 1.062−2.020, p = 0.020; AOR = 2.677, 95% CI = 1.066−6.725, p = 0.036, respectively). We further propose that miR-10aA\u3eT, miR-30cA\u3eG, and miR-499bA\u3eG polymorphisms effects could contribute to RPL and should be considered during RPL patient evaluation

Hepatocellular adenoma in a Eurasian otter (Lutra lutra)

A 7-year-old female Eurasian otter (Lutra lutra) at the Seoul Grand Park, Korea, died after displaying depression, anorexia, weight loss and rough skin for several days. At necropsy, a solitary friable round mass, which was approximately 12 × 9 × 5 cm and mottled dark red and yellow, was found bulging from the right hepatic lobe. Microscopically, the nonencapsulated, poorly circumscribed mass was composed of solid sheets of neoplastic hepatocytes. In addition, numerous small tan foci, ranging from 0.5 to 1.0 cm in diameter, were evenly scattered throughout the pancreatic tissue. These foci were found to be nonencapsulated, well-demarcated hyperplastic nodules of the exocrine pancreatic gland. We observed neither intrahepatic nor extrahepatic metastases. Based on the gross and microscopic changes, we diagnosed the animal as having a hepatocellular adenoma accompanied by exocrine pancreatic nodular hyperplasia

Connexin32 inhibits gastric carcinogenesis through cell cycle arrest and altered expression of p21Cip1 and p27Kip1

Gap junctions and their structural proteins, connexins (Cxs), havebeen implicated in carcinogenesis. To explore the involvement ofCx32 in gastric carcinogenesis, immunochemical analysis of Cx32and proliferation marker Ki67 using tissue-microarrayed humangastric cancer and normal tissues was performed. In addition, afterCx32 overexpression in the human gastric cancer cell line AGS,cell proliferation, cell cycle analyses, and p21Cip1 and p27Kip1expression levels were examined by bromodeoxyuridine assay,flow cytometry, real-time RT-PCR, and western blotting.Immunohistochemical study noted a strong inverse correlationbetween Cx32 and Ki67 expression pattern as well as theirlocation. In vitro, overexpression of Cx32 in AGS cells inhibitedcell proliferation significantly. G1 arrest, up-regulation of cellcycle-regulatory proteins p21Cip1 and p27Kip1 was also found atboth mRNA and protein levels. Taken together, Cx32 plays someroles in gastric cancer development by inhibiting gastric cancercell proliferation through cell cycle arrest and cell cycle regulatoryproteins. [BMB Reports 2013; 46(1): 25-30