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Fourteen guinea pigs were given prednisolone daily for 20 days and 11 for 40 days. Another 20 formed the two control groups. Short-term prednisolone treatment significantly increased serum gastrin levels and antral G-cell population as compared to the control group. The same parameters significantly decreased following 40 days of prednisolone treatment as compared to the group of short-term prednisolone treatment. Forty days of prednisolone treatment significantly increased antral D-cell population as compared to the control and short-term prednisolone treatment groups. It is concluded that hypergastrinaemia and antral G-cell hyperplasia following corticosteroid administration is temporary and is accompanied by antral D-cell hyperplasia.

In the present study antral G-cells which secrete gastrin and antral and fundic D-cells which secret somatostatin, an inhibitor of gastric acid secretion were revealed immunocytochemically and the population size estimated along with serum gastrin levels in ten male and eight female guinea pigs. Serum gastrin, antral G-cells, antral D-cells and fundic D-cells were 41.90 +/- 6.10 SD pg/ml, 210 +/- 18.03 SD cells/cm, 128.20 +/- 17.64 SD cells/cm and 121 +/- 17.91 SD cells/cm respectively in males and 35 +/- 4.62 SD pg/ml, 176 +/- 13.80 SD cells/cm, 108.40 +/- 6.90 SD cells/cm and 106.8 +/- 6.50 SD cells/cm respectively in females. The differences in serum gastrin levels, antral G-cell population and antral D-cell population between the two sexes were statistically significant (P less than 0.05, P less than 0.001, P less than 0.01). It is possible that endogenous androgens induce a relative hyperplasia and endogenous oestrogens a relative hypoplasia of G-cells. Antral D-cell differences may reflect an adaptive hormonal mechanism to the possible different states of gastric secretory functions.

Twelve dogs underwent an extensive proximal small bowel resection. Basal and postprandial serum gastrin levels increased significantly one and two months after the resection compared to the respective preoperative levels. The increase in serum gastrin levels two months after the resection was less prominent than the respective increase one month postoperatively. Antral G- and D-cell populations increased significantly two months after the resection compared to the respective populations before the resection. It is concluded that hypergastrinaemia following small bowel resection is due to the quantitative elimination of the inhibiting hormonal factors of gastric secretion and gastrin release. The adaptive increase of antral D-cell population could explain the temporary character of hypergastrinaemia.

Twelve female guinea pigs were given estradiol and another 12 testosterone for 18 days. A third group of 15 animals underwent oophorectomy and a group of 8 animals served as controls. Gastric and pancreatic D-cells were quantitated in all four groups. Oophorectomy and androgens significantly increased and estrogens significantly decreased gastric D-cell populations. Additionally, estrogens significantly decreased D-cell population in pancreatic islets. It is concluded that the alterations in gastric and pancreatic D-cell populations, which are induced by sex hormone administration and oophorectomy, possibly reflect a hormonal adaptive attempt to restore gastric secretory functions within the normal range.