Production of bacteriocin by Leuconostoc mesenteroides 406 isolated from Mongolian fermented mare's milk, airag.

The purification and characterization of a bacteriocin produced by Leuconostoc mesenteroides strain 406 that was isolated from traditional Mongolian fermented mare's milk, airag, were carried out. Leuconostoc mesenteroides strain 406 was identified on the basis of its morphological and biochemical characteristics and carbohydrate fermentation profile and by API 50 CH kit and 16S ribosomal DNA analyses. The neutral-pH cell-free supernatant of this bacterium inhibited the growth of several lactic acid bacteria and food spoilage and pathogenic organisms, including Listeria monocytogenes and Clostridium botulinum. The bacteriocin was heat-stable and not sensitive to acid and alkaline conditions, but was sensitive to several proteolytic enzymes such as pepsin, pronase E, proteinase K, trypsin, and α-chymotrypsin, but not catalase. Optimum bacteriocin production (4000 activity units/mL) was achieved when the strain was cultured at 25°C for 24-36 h in Man Rogosa Sharpe medium. The bacteriocin was partially purified by ammonium sulfate precipitation (80% saturation), dialysis (cut-off MW: 1000), and gel filtration chromatography. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed that the bacteriocin had a molecular weight of approximately 3.3 kDa. To our knowledge, this is the first report of the isolation of a bacteriocin-producing Leuconostoc strain from airag. An application to fermented milks would be desired.

Serum free testosterone and metabolic syndrome in Japanese men.

To examine the association between late-onset hypogonadism (LOH) and metabolic syndrome (Mets) or insulin resistance in the Japanese adult male population, we evaluated anthropometric parameters, indices of glucose and lipid metabolism, and hormones related to sexual function in 274 men (mean age: 46.0 +/- 11 years) who underwent general health checks. Seventy subjects (25.5%) were diagnosed as having Mets, while the frequency of LOH was 8.0%. Glycated hemoglobin was normal in the majority of participants (94.9%). The serum free testosterone (FT) level was significantly lower in the Mets (+) group than in the Mets (-) group (11.7 +/- 4.0 vs. 14.7 +/- 4.6 pg/mL, p<0.0001). FT decreased significantly along with an increase in the number of Mets components. Likewise, the number of Mets components showed a significant difference among the eugonadal, borderline, and hypogonadal groups (2.2 +/- 1.4, 1.5 +/- 1.4, and 0.9 +/- 1.1, respectively). After adjustment for age, body mass index (BMI), and waist circumference (WC), FT was still significantly correlated with Mets (standard partial regression coefficient = - 0.0971; 95 % confidence interval = - 0.1936 approximately - 0.0006; p = 0.048). A compensatory increase of gonadotropins was not seen in the hypogonadal group. Among Japanese men who were mainly without diabetes, FT was associated with Mets independently of age, BMI, and WC. Mets and insulin resistance may decrease serum testosterone via induction of hypogonadotrophic hypogonadism, and the reduction of testosterone may in turn cause further obesity and insulin resistance, consequently initiating a vicious cycle.

A mitochondrial DNA variant associated with left ventricular hypertrophy in diabetes.

Diabetes was reported to be associated with a mitochondrial (mt) DNA mutation at 3243 and variants at 1310, 1438, 3290, 3316, 3394, 12,026, 15,927, and 16,189. Among these mtDNA abnormalities, those at 3243, 3316, 15,927, and 16,189 were also suggested to cause cardiomyopathies. We investigated the prevalence of such mtDNA abnormalities in 68 diabetic patients with LV hypertrophy (LVH), 100 without LVH, and 100 controls. Among the 9 mtDNA abnormalities, those at 3243, 3316, and 15,927 tended to be more prevalent in diabetic patients with LVH than in those without LVH (1%, 1%, and 4% vs. 0%, 0%, and 0%). Notably, the variant at 16,189 was more prevalent in diabetic patients with LVH than without LVH (46% vs. 24%, [Formula: see text] ). The odds ratio for LVH was 3.0 (95% CI, 1.5-6.1) for the 16,189 variant. A common mtDNA variant at 16,189 was found to be associated with LVH in diabetic patients.