We have already reported that slowly progressive non-insulin-dependent diabetes mellitus (NIDDM) is produced by a single i.p. injection of a subdiabetogenic dose (100 mg/kg) of streptozotocin (STZ) to 8-week-old male ICR mice. The aim of the present study was to clarify whether or not the progressive NIDDM is induced in ddY, BALB/c, C57BL/6 and ICR mice by the administration of STZ. Eight-week-old male mice of the 4 different strains were administered a single i.p. injection of STZ at various doses (ICR, ddY and BALB/c: 100-200 mg/kg; C57BL/6: 75-150 mg/kg). Among the ddY, BALB/c and C57BL/6 mice, a time course-related rise in non-fasting serum glucose levels throughout the observation period of 1-12 weeks after STZ administration was only induced in the 125 mg/kg STZ ddY and 100 mg/kg STZ ICR mice. In contrast with serum glucose levels, the area of islets and the percentage of the relative number of insulin-immunoreactive cells (b b-cells) to glucagon-immunoreactive cells (a a-cells) in the 100 mg/kg STZ ICR and 125 mg/kg STZ ddY mice continued to decrease gradually over time. In addition, in low dose STZ mice of both strains, the insulin response to glucose stimulation was extremely impaired over time, although non-fasting serum insulin levels were maintained near normal levels. The rate of the progression of diabetes was faster in the 125 mg STZ ddY mice than in the 100 mg/kg STZ ICR mice.

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This article develops a non-Bayesian methodology to analyse the time-varying structure of international linkages and market efficiency in G7 countries. We consider a non-Bayesian time-varying vector autoregressive (TV-VAR) model, and apply it to estimate the joint degree of market efficiency in the sense of Fama (1970, 1991). Our empirical results provide a new perspective that the international linkages and market efficiency change over time and that their behaviours correspond well to historical events of the international financial system.

Diabetes mellitus is classified into two types, type 1 (insulin-dependent) and type 2 (non-insulin-dependent). Type 2 diabetes mellitus is divided into two categories, obese type with hyperinsulinemia and non-obese type with hypoinsulinemia. It is established that obesity causes peripheral insulin resistance which leads to hyperinsulinemia. Obesity-related type 2 diabetes mellitus is also characterized by hypertriglyceridemia as well as hyperinsulinemia.1) It is clear from a number of clinical and experimental studies that triglyceride production is increased in hyperinsulinemia.2,3) Man et al. 4) have demonstrated that hypertriglyceridemia in non-insulin-dependent diabetes mellitus (NIDDM)-prone OLETF rats results in a high triglyceride content in islets. 4) They suggest that fat droplets in islets may play an important role in hastening the development of NIDDM in this model by the impairment of pancreatic b-cell function. Therefore, the above findings strongly suggest that improving the abnormality of lipid metabolism as well as glucose metabolism may be useful in preventing the development or progression of obesity-related type 2 diabetes mellitus.Chitosan is chemically a polymeric D-glucosamine, a basic polysaccharide, and is produced by deacetylating chitin, a polymeric N-acetyl-b-D-glucosamine, with 40-45% NaOH at 120°C (Fig. 1).5) Chitin is insoluble in water, acid or alkaline solution. However, chitosan is easily solubilized in acid solution, because it has amino groups in its chemical structure. It has been reported that chitosan has many pharmacological actions such as immunopotentiating, 6,7) anti-hypertensive, 8) serum cholesterol-lowering, 9-11) anti-bacterial, 12,13) and wound healing-promoting actions. [14][15][16] In our previous study, we reported that chitosan (MW: 25000-50000) has potent gastric cytoprotective and ulcerhealing promoting actions in rats.17) Miura et al. 18) first showed that chitosan given as a 5% food mixture produces consistent blood glucose-and lipid-lowering effects in normal mice and neonatal streptozotocin (STZ)-induced diabetic mice, one of the animal models of non-obese type NIDDM, but this compound is ineffective in improving these biochemical parameters in KK-A y mice, one of the animal models of genetically obese type NIDDM with hyperinsulinemia. Recently, we succeeded in creating a new mouse model of slowly progressive NIDDM by only a single i.p. injection of a subdiabetogenic low dose (100 mg/kg) of STZ to 8-weekold male ICR mice. 19,20) We reported that low molecular weight (LMW) chitosan (chitosan lactate, average MW: 20000) prevented the progression of low dose STZ-induced slowly progressive NIDDM.21) Therefore, in the present study, we examined the effect of the long-term administration of LMW chitosan, given as drinking water, on hyperglycemia, hyperinsulinemia and hypertriglyceridemia of diabetes mellitus in male KK-A y mice, an animal model of genetically obese-type NIDDM. MATERIALS AND METHODSAnimals Five-week-old male KK-A y (Clea, Tokyo, Japan) and mal...