In developed and developing countries, morbidity and mortality rates are increasing in individuals classified as being obese [1-6]. The higher morbidity and mortality rates of obese people are due to the increased incidence of obesity-related (lifestyle-related) diseases. It is now recognized that different criteria of obesity by BMI are necessary in different ethnic groups and populations [7,8]. In addition to the degree of obesity, other factors which increase the morbidity rate of obese people include abnormal fat distribution such as upper body obesity and visceral obesity [9,10]. Recently, the definition of 'pathological obesity' has been made in Japan [11]. Definition of Obesity and Previous Criteria of ObesityObesity is defined as excessive fat accumulation but not over-weightedness. The average human body usually consists of 82% lean body mass, which is essential for sustaining daily life and physical activities, and 18% body fat which, in essence, is energy store for emergency situations [12]. Thus, obesity can be defined as 'overstorage of body fat beyond 18%'. Usually, body fat above 25% in men and 30% in women is considered to be obese. According to this definition, obesity should be determined by measuring body fat. Although there are presently many methods for measuring body fat, no methods can be conducted easily, accurately and inexpensively.

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Abstract.Diabetes mellitus in Long-Evans Tokushima Lean (LETL) rats closely resembles type 1 diabetes in human beings, e.g., no gender differences in the incidence of diabetes and no T lymphopenia. Although the LETL rats have been established as an inbred strain, the incidence of diabetes is only '2O%. In the present study, we established two substrains, one a diabetes-prone (KDP) and the other a nondiabetic (KND) from the original inbred LETL rats. The features of KDP rats are a high incidence of diabetes (over all -7O%) without lymphopenia and 100% development of mild to severe insulitis at 120-220 days of age. In contrast, the KND substrain is characterized by the complete absence of diabetes incidence. Among 165 SSLP marker loci throughout all rat chromosomes, no loci showed variation among KDP and KND substrains and their parental LETL rats. In this regard, the genetic background of these two substrains, KDP and KND, appears to be uniform except for the major gene(s) that is responsible for the diabetes. In this context, these two substrains of LETL rats should serve as useful tools for research on the pathogenesis and for the genetic analysis of type 1 diabetes. In this report, we have not only established, but also characterized these two substrains, and provided their fundamental data.

Aims/IntroductionDiabetes mellitus and periodontitis are closely related. A huge number of reports has addressed the effect of periodontal intervention therapy on glycemic control, but no reports have addressed the effect of glycemic intervention therapy on periodontal disease in type 2 diabetic patients. The aim of this study was to examine the effect of improved glycemic control by glycemic intervention therapy on periodontitis in type 2 diabetic patients.Materials and MethodsA total of 35 patients underwent intervention therapy to improve glycemic control without periodontal treatment. Glycohemoglobin (HbA1c), high-sensitivity C-reactive protein (hs-CRP), bleeding on probing (BOP), probing pocket depth (PPD) and intraoral community periodontal index (CPI) codes of the World health Organization (WHO) were examined at baseline, and 2 and 6 months after the intervention therapy to improve glycemic control.ResultsAfter the improvement of glycemic control, BOP lesions improved, but deep PPD lesions and WHO CPI codes did not improve. Subanalyses showed that effective glycemic control (average HbA1c reduction 1.8%) improved BOP lesions, but did not affect deep PPD lesions and WHO CPI codes. In addition, high BOP lesions at baseline responded more effectively to glycemic intervention. Further analysis of CPI codes in all individual periodontal sites independent of WHO CPI codes in 35 patients showed that only gingival inflammation without a deep periodontal pocket improved after glycemic intervention.ConclusionsEffective glycemic control improves BOP lesions in type 2 diabetic patients with periodontitis through ameliorating inflammation at the gingival sites of periodontal tissue. This trial was registered with the University Hospital Medical Information Network (no. UMIN000007670).