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S. Kasayama, M. Yoshimura, and T. Oka


The effects of androgen and thyroid hormones on epidermal growth factor (EGF) synthesis in the submandibular gland and on plasma EGF concentrations in mice were examined. Testosterone propionate was administered alone or in combination with l-thyroxine (T4) to female mice for 2 weeks. The submandibular EGF concentrations were increased by the administration of testosterone propionate in a dose-dependent fashion; the maximal increase, 20-fold, being produced by a dose of 2 mg every other day. The EGF levels were increased sevenfold by T4, which also enhanced the stimulatory effect of suboptimal doses of testosterone propionate. Cyproterone acetate, an anti-androgen, inhibited the testosterone propionate-induced increase, but not the T4-induced increase. Plasma EGF concentrations were raised by testosterone propionate but not by T4. Both hormones stimulated the accumulation of 4·7 kb preproEGF mRNA in the submandibular gland, which occurred almost in a parallel manner with the increase in submandibular EGF concentrations. These results suggest that EGF synthesis in the submandibular gland is regulated by alterations in the level of its mRNA by thyroid hormones and androgen, and that the rise in plasma EGF concentrations is under the influence of androgen but not of thyroid hormones.

Journal of Endocrinology (1989) 121, 269–275

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S. Sakuma, N. Shirasawa, and F. Yoshimura


Two weeks after operation the effects of castration on all types of mitotic adenohypophysial cells in 30-day-old (immature) and 75-day-old (mature) male rats were studied immunohistochemically by light microscopy. The total number of mitotic cells in gland specimens increased 1·4 times in immature rats, but remained unchanged in mature animals; mitotic activity (mitotic cell number/mm2) was not affected in either age group. The population of mitotic gonadotrophs increased five to six times in comparison with intact controls. In addition, the percentage of mitotic gonadotrophs and their mitotic activity were raised in both age groups. Castration affected the mitosis of prolactin cells. The percentage of mitotic prolactin cells was reduced by one-third in castrated immature rats, but the total number and percentage of mitotic prolactin cells, as well as their mitotic activity, was reduced by about two-thirds in mature castrated rats. No significant changes in mitotic ACTH, TSH, GH and immunonegative cells were found after castration in either group of animals.

Mitotic cells were more numerous in the anterior than in the posterior region of the gland in normal (uncastrated) immature rats, but were uniformly scattered in both regions in normal mature rats. On the other hand, castration induced a high population of mitotic cells in the anterior region regardless of age. This high population was the result of the enhanced mitosis of gonadotrophs. It is concluded that 2 weeks after castration the increment of mitotic divisions of all types of pituitary cells is age-dependent, and that mitosis takes place frequently in gonadotrophs and less frequently in prolactin cells.

J. Endocr. (1984) 100, 323–328

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J. Kawada, M. Okita, M. Nishida, Y. Yoshimura, K. Toyooka, and S. Kubota


Ethylidene glucose (4,6-O-ethylidene glucose; EG) is known to bind the outer surface of the glucose transporter in the membranes of human erythrocytes and other mammalian cells. If a glucose transport system is present on pancreatic β cells and recognizes the glucose moiety of streptozotocin (STZ), EG should protect β cells from the cytotoxicity of STZ when it is administered with STZ. This possibility was examined in in-vivo experiments in rats. When EG and STZ were injected into rats together the animals did not become diabetic, as judged by (1) their blood glucose levels, (2) response in a glucose-tolerance test, and (3) insulin secretion in response to feeding. These results suggest that there is a glucose transporter present in β cells and also the transport of streptozotocin into β cells through this system.

J. Endocr. (1987) 112, 375–378

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R Kurotani, S Yoshimura, Y Iwasaki, K Inoue, A Teramoto, and RY Osamura

The pituitary-specific POU-homeodomain transcription factor, Pit-1, is known to regulate the expression of the GH gene in somatotropes, prolactin (PRL) in lactotropes, and TSH in thyrotropes. It is not normally expressed in corticotropes or gonadotropes. We addressed the question of whether exogenous Pit-1 was sufficient to induce ectopic transcription of the GH gene in the corticotropic cell line, AtT-20, or the gonadotropic cell line, alpha T3-1. A fusion gene composed of enhanced green fluorescent protein gene and human Pit-1 cDNA was transfected into AtT-20 and alpha T3-1 cells. The endogenous mouse GH mRNA was induced in three of nine AtT-20 cell lines and one of three alpha T3-1 cell lines containing the fusion gene. A small amount of GH protein was also detected in these cell lines. These data indicate that transfected Pit-1 is capable of inducing transcription of the GH gene in AtT-20 cells and alpha T3-1 cells. These data also suggest that synergistic co-factors might be required to transcribe the GH gene effectively for translation into GH protein. Furthermore, our findings support the hypothesis that the function of anterior pituitary cells is determined by the combinatorial action of specific transcription factors.