Kumiko Minato

The effect of chronic exercise on the rat pancreas

SummaryBackground. We recently demonstrated that chronic physical exercise increases pancreatic protein content and basal amylase secretion. It is unknown whether chronic exercise causes hypertrophy or proliferation of pancreatic acinar cells. Methods. Female F344 rats (age, 6 wk) were divided into control (n= 7) and exercise (n=6) groups. Food consumption was matched between the 2 groups. Rats in the control group were kept sedentary. Rats in the exercise group were exercised for 60 min, 5 d/wk during the experiment. After 8 wk, the pancreas and hindlimb muscles were rapidly excised and weighed. Protein and DNA content and enzyme activity in pancreatic tissue were measured. Pancreatic tissues from control and exercised rats were also prepared for transmission electron microscopy. Results. Inhibition of growth and hypertrophy of hindlimb muscles were exhibited by the exercise group. In the exercise group, pancreatic wet weight, protein content, and amylase and lipase activities, but not DNA content, were significantly higher than those in the control group. Electron micrographs clearly revealed that acinar cells were hypertrophied and zymogen granules were increased in number in exercised rats.Conclusion. Chronic endurance exercise increases pancreatic weight, protein content and enzyme activity through hypertrophy of acinar cells.

Effect of endurance training on pancreatic enzyme activity in rats

Abstract The effect of chronic exercise on pancreatic enzyme activity and basal pancreatic secretion was investigated in rats. Male Wistar rats were divided into three groups of ten rats each. In a trained (T) group, the animals were exercised on a treadmill at 35 m · min−1 for 60 min, 5 days · week−1. A free-fed control (C) group and a pair-fed control (PFC) group were kept sedentary. Food intake in the PFC group was restricted to the T group levels. After 6 weeks, pancreas wet mass per unit of body mass was significantly larger in the T group in comparison to the C and PFC groups. Protein content, and amylase and lipase activities of the pancreas were significantly higher in the T group in comparison to the C and PFC groups. Basal amylase but not bile-pancreatic juice volume was higher in the T group than in the other two groups. There were no significant differences between groups C and PFC in any of the above parameters. These results would suggest that pancreatic enzyme synthesis and basal secretion are accelerated with physical endurance training. This adjustment would be a beneficial adaptation to chronic endurance exercise, which requires a large energy supply from food.

The Exercise-Induced Improvement in hyperglycemia is Mediated by DHT Produced in the Skeletal Muscle of Zucker Diabetic Fatty Rats

The ability of exercise to improve hyperglycemia by enhancing glucose metabolism in the skeletal muscle of type 2 diabetic patients is well established. We reported sex steroid hormones can be locally synthesized in skeletal muscle and decrease fasting blood glucose levels in obese rats. Here, we determined whether exercise-induced production of sex steroid hormones in skeletal muscle could directly reverse hyperglycemia in the Zucker diabetic fatty rat model using osmotic mini pump. Thirty Zucker diabetic fatty rats were randomly assigned to the following groups: control, exercise, or exercise with continuous infusion of 5α-reductase inhibitor. The results indicated 6 weeks of exercise significantly reduced serum insulin and fasting glucose levels compared to control group. Dehydroepiandrosterone, 5α-dehydrotestosterone, and 5α-reductase levels were all significantly higher in skeletal muscle of the exercise group. Moreover, exercise increased glucose transporter-4 translocation with a concomitant upregulation of phosphorylated phosphoinositide 3-kinase, protein kinase B and C-ζ/λ. Furthermore, significant correlations were observed between fasting glucose and muscular DHT levels. Interestingly, the observed exercise-induced improvements in serum insulin and fasting glucose levels were all suppressed by administration of 5α-reductase inhibitor. These results indicated the exercise-induced improvements in glucose metabolism signaling and glucose levels may be directly attributed to the increased levels of sex steroid hormones within skeletal muscles.

Characterization of fat metabolism in the fatty liver caused by a high-fat, low-carbohydrate diet: A study under equal energy conditions

The pathology of fatty liver due to increased percentage of calories derived from fat without increased overall caloric intake is largely unclear. In this study, we aimed to characterize fat metabolism in rats with fatty liver resulting from consumption of a high-fat, low-carbohydrate (HFLC) diet without increased caloric intake. Four-week-old male Sprague-Dawley rats were randomly assigned to the control (Con) and HFLC groups, and rats were fed the corresponding diets ad libitum. Significant decreases in food intake per gram body weight were observed in the HFLC group compared with that in the Con group. Thus, there were no significant differences in body weights or caloric intake per gram body weight between the two groups. Marked progressive fat accumulation was observed in the livers of rats in the HFLC group, accompanied by suppression of de novo lipogenesis (DNL)-related proteins in the liver and increased leptin concentrations in the blood. In addition, electron microscopic observations revealed that many lipid droplets had accumulated within the hepatocytes, and mitochondrial numbers were reduced in the hepatocytes of rats in the HFLC group. Our findings confirmed that consumption of the HFLC diet induced fatty liver, even without increased caloric intake. Furthermore, DNL was not likely to be a crucial factor inducing fatty liver with standard energy intake. Instead, ultrastructural abnormalities found in mitochondria, which may cause a decline in β-oxidation, could contribute to the development of fatty liver.

A System for Nutritional Consulting Using Quick Questionnaires on Diet and Unidentified Complaints

The aging of society and ongoing health care cost-control policy set the trend for the self-medication which leads to the growing interest in health promotion and prolongation of healthy life expectancy through self-health management. We developed a self-medication support system to provide comprehensive support to consumers at pharmacies and drug stores. This system facilitates the effective use of information and knowledge based on medicine and health. This self-medication support system comprised a set of two terminals connected network server in the data center: a user terminal for consumers use and an advisor terminals for specialized advisor, pharmacists, registered dieticians, and etc. This system enables specialized sales people to provide the appropriate advice based on the factors of consumer’s problem, and to make suggestions for improving his/her lifestyle: eating habit, doing exercise, and having relaxation time. As a result of the trial use of this system at pharmacy stores, a certain degree of correlation between the results of a questionnaire on unidentified complaints and dietary patterns causing potential micronutrient deficiency was demonstrated.