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Biomedical subjects

G Yoshino

Publications and source records attributed to G Yoshino.

8 recordsLinked to original sources
PubMed1979

Insulin and glucagon relationships during aging in rats.

Oral glucose tolerance tests were performed under pentobarbital anesthesia in 43 male Wistar rats 2 to 18 months of age in order to determine if insulin and glucagon secretion are altered with aging. Although any linear correlation was not demonstrated between aging and blood glucose, plasma insulin or glucagon levels, post-glucose levels of blood glucose were significantly suppressed and those of plasma glucagon were significantly elevated at 4 to 6 months of age. No significant difference was found between young (2 months of age) and aged rats (12 to 14 and 17 to 18 months of age) in either blood glucose or plasma insulin levels during oral glucose load. On the other hand, post-glucose plasma glucagon levels of the aged rats were significantly higher than those of the young ones. Furthermore, comparisons of various kinds of indices among the different age groups, such as insulinogenic index, insulin/glucagon and so forth during oral glucose tolerance tests also indicate the significant alteration of glucagon secretion during aging process. It is concluded from the present data that glucose tolerance does not apparently deteriorate during aging process in rats but that glucagon responses to oral glucose administration are elevated with aging.

Aging↗
PubMed1979

Glucagon secretion during the development of insulin-secreting tumors induced by streptozotocin and nicotinamide.

Serial oral glucose tolerance tests in rats treated with streptozotocin and nicotinamide showed that blood glucose levels after glucose loading were suppressed significantly 7 months after treatment as compared to those of earlier stages. Post-glucose plasma insulin levels were significantly elevated at the 9th to 12th month and concomitantly fasting plasma glucagon levels rose significantly. At that time pancreatic islet cell tumors were demonstrated in all of the rats in this experiment. Post-glucose plasma glucagon levels, however, did not show remarkable changes throughout the observation. In spite of hyperinsulinemia, post-glucose plasma glucagon levels of tumor-bearing rats were significantly lower than those of body weight adjusted controls. It is inferred from the study that secretory activity of pancreatic A-cells of tumor-bearing rats is restrained by excess insulin released from islet cell tumors.

Adenoma, Islet Cell↗
PubMed1978

Biochemical studies on rats with insulin-secreting islet cell tumors induced by streptozotocin: with special reference to physiological response to oral glucose load in the course of and after tumor induction.

Pancreatic islet cell tumors were induced in 32 of 49 male Wistar rats (73%) surviving 9 months or longer following treatment with streptozotocin alone, with streptozotocin and nicotinamide, or with streptozotocin and picolinamide. Serial oral glucose tolerance tests in rats treated with streptozotocin and nicotinamide showed that the elevation of blood glucose levels after oral glucose load was depressed significantly 7 months after treatment. Plasma insulin responses were distinctly elevated 9 months after treatment. Blood glucose levels remained lower and plasma insulin levels rose markedly after a glucose load in tumor-bearing rats as compared to the response of tumor-free rats. These findings suggest that pancreatic islet cell tumors induced by streptozotocin with and without combined treatment are insulin-secreting, and that streptozotocin itself has oncogenic effects on the rat pancreas. Mean insulin concentration in islet cell tumors amounted to 401 U/g wet wt, whereas the concentration was 14 U/g wet wt in the pancreatic tissue from tumor-free rats.

Adenoma, Islet Cell↗
PubMed1978

Tumorigenic action of streptozotocin on the pancreas and kidney in male Wistar rats.

Pancreatic islet cell tumors were induced in 38 of 44 male Wistar rats (86%), which survived 9 to 14 months following the various treatment schedules. A single i.v. injection of streptozotocin alone, 30, 40, 50, or 65 mg/kg of body weight produced adenomas of pancreatic islet cells in 8 of 9 (89%), 6 of 7 (86%), 2 of 4 (50%), and 1 of 2 rats (50%), respectively. The neoplasms were seen in all of the 8 rats given a single i.p. injection of picolinamide, 250 mg/kg of body weight, 15 min before a single i.v. injection of streptozotocin, 65 mg/kg of body weight. Among the 14 rats given a single i.p. injection of nicotinamide, 500 mg/kg of body weight, 15 min before a single i.v. injection of streptozotocin, 65 mg/kg of body weight, 13 rats (95%) developed pancreatic islet cell tumors. Renal tumors were seen in only 3 rats treated with streptozotocin and nicotinamide. None of rats used in this study developed hepatic tumors. This study demonstrates that steptozotocin, even in a dose of 30 mg/kg of body weight, has an exceedingly marked tumorigenic action on the rat pancreas, while it has little effect on the kidney and no effect on the liver.

Adenoma, Islet Cell↗