Specific mitochondrial DNA mutation in mice regulates diabetes and lymphoma development

It has been hypothesized that respiration defects caused by accumulation of pathogenic mitochondrial DNA (mtDNA) mutations and the resultant overproduction of reactive oxygen species (ROS) or lactates are responsible for aging and age-associated disorders, including diabetes and tumor development. However, there is no direct evidence to prove the involvement of mtDNA mutations in these processes, because it is difficult to exclude the possible involvement of nuclear DNA mutations. Our previous studies resolved this issue by using an mtDNA exchange technology and showed that a G13997A mtDNA mutation found in mouse tumor cells induces metastasis via ROS overproduction. Here, using transmitochondrial mice (mito-mice), which we had generated previously by introducing G13997A mtDNA from mouse tumor cells into mouse embryonic stem cells, we provide convincing evidence supporting part of the abovementioned hypothesis by showing that G13997A mtDNA regulates diabetes development, lymphoma formation, and metastasis--but not aging--in this model.     

住院患者入院时血糖水平与医疗费用、疾病预后的相关研究

目的探讨住院患者人院时不同血糖水平与住院时间、医疗费用及疾病预后的关系。方法选取2009年11月至2011年7月期间人院的4868例患者,按入院24h内测得的血糖水平分为非高血糖组3429例、高血糖组1439例,后者包括糖尿病和应激性高血糖患者;根据患者年龄分为非老年组（年龄〈60岁）2532例和老年组（年龄≥60岁）2336例;其中278例冠心病患者再分为高血糖组120例和非高血糖组158例。各组间进行有关数据比较。结果高血糖组患者的住院天数、医疗费用和总病死率均显著高于非高血糖组（中位数住院日：15vs10d,P〈0．01;中位数医疗费用：14064．7vs8980．9元,P〈0．01;死亡率：2．92％vs0．61％,P〈0．01）。按年龄分组后,无论是非老年组还是老年组中糖尿病和应激性高血糖患者的医疗费用均明显高于非高血糖患者,住院日明显延长;应激性高血糖患者的医疗费用明显高于糖尿病患者;非老年组中应激性高血糖患者的死亡率明显高于非高血糖患者,但与糖尿病患者相比无明显差异,老年组糖尿病和应激性高血糖患者的死亡率无明显差异,但均明显高于非高血糖患者。冠心病患者中糖尿病和应激性高血糖患者与非高血糖患者的年龄无明显差异,前两组的医疗费用明显高于非高血糖组,住院日更长（分别为14,15和12d）、死亡率更高（分别为6．41％,7．14％和0．63％）。结论入院时高血糖水平预示患者有更高的医疗花费、更长的住院时间和更高的死亡率。     

Tooth and periodontal clinical attachment loss are associated with hyperglycemia in patients with diabetes

Background: Periodontal disease has been associated with diabetes, but there is still controversy on the relationship between periodontal clinical parameters and glycemic control. The purpose of this study is to assess the relationship between blood glucose levels and clinical parameters of periodontal disease in individuals with diabetes. Methods: A total of 65 individuals with diabetes and 81 individuals without diabetes were included in the study. A full-mouth periodontal examination and preprandial fasting glycemia values were recorded for each individual. Glycosylated hemoglobin was only measured in patients with diabetes. A comparative analysis between groups (Mann-Whitney U test) and a correlation analysis between glycemia and periodontal parameters were performed (Spearman test). Results: Patients without diabetes presented more teeth than individuals with diabetes (P <0.05). Patients with diabetes with periodontitis displayed loss of periodontal clinical attachment compared to patients without diabetes, but the highest value was observed in patients with periodontitis that reported a smoking habit. Furthermore, patients with diabetes with periodontitis presented higher glycemia and glycated hemoglobin values in contrast to patients with gingivitis. Patients with diabetes with hyperglycemia had a higher risk to develop periodontitis (odds ratio = 2.24; 95% confidence interval = 1.02 to 4.93). A positive correlation was observed between glycemia and clinical attachment loss (AL), whereas a negative correlation between glycemia and the number of teeth present was found (P <0.05). Conclusions: Tooth and periodontal AL were increased by hyperglycemia in individuals with diabetes. This study contributes additional evidence that diabetes could aggravate periodontal disease and affect the systemic health of individuals.