Case 1.
1. Female patient, aged 60, suffering from Acromegaly since about 25 years ago, complicated with diabetes mellitus 2 years ago. The authors chiefly studied the pathogenesis of this particular diabetes.
2. The occurrence of this particular diabetes appears to involve various pancreatic factors, in addition to extra pancreatic factors. In other words, the case is diagnosed as socalled insulin resistant pluriglandular type of diabetes that has low function of Langerhans'islets in pancreas accompanied with hyperfunction of anterior pituitary.
3. In the pituitary adrenocortical function' tests, the result of Thorn's test was markedly abnormal, the steroid hormones excretion in the urine by ACTH administration increased considerably and the blood sugar curve resembled that of pluriglandular diabetes.
Case 2.
4. Male patient, aged 64, Acromegalia complicated with diabetes 8 years ago.
The authors studied the pathogenesis of this particular diabetes.
5. The patients was found to be relatively severe state at the time of admission. The patient left the hospital without any improvement of sugar regulatory function, and with the accelerated sugar producing capacity, and with insulin resistence, in spite of 20 days dietary treatement during admission.
6. In the pituitary adrenocortical function tests, the result of Thorn's test was normal, the steroid hormones excretion in the urine by ACTH administration increased remakably and the fall of blood sugar values by ACTH administration was slightly, on the other hand, it was remarkable by cortisone administration.
From above mentioned studies, the authors conclude as follows; Steroid hormones excretion in the urine by ACTH administration and blood sugar curve by three kinds of hormones (ACTH. cortisone, and DCA) are necessary to verify the clinical classification of this type of diabetes.

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In order to study the effects of various steroid hormones on the thyroid gland of normal and hypophysectomized adult rats, histological and physiological investigations were carried out by means of isotope I¹³¹.
Testosterone propionate, methyltestosterone (2 and 2.5mg intramuscular, daily) and methyl-androstenediol (1, 5 and 10mg intramuscular or per os, daily) were separately administered for 15-37 days. In normal rats, proliferation as struma parenchymatosa was observed and thyroid weight, mitotic activity, RNA content of epitheliar cell, I¹³¹ uptake by thyroid and protein bound I¹³¹ (PBI¹³¹) content of plasma were all increased. Therefore, these hormones were supposed to promote the thyroid activity. In hypophysectomized rats, also, mitotic figures of epitheliar cell were observed when examined with colchitin, and increase of thyroid weight,I¹³¹ uptake by thyroid and PBI¹³¹ content of plasma was prominent in hormone treated group.Above androgens might, therefore, be considered to stimulate the thyroid epithel and to promote the thyroid function moderately, without hypophysis.
Hexesterol of 5 gamma per day for 10 days raised the percentage of I¹³¹ accumulated inthyroid gland, both in normal and hypophysectomized rats.
When estradiol of 15, 30, 50 and 100 gamma per day was injected for 10-30 days, thyroid weight and histological proliferation increased in proportion to dosage. However, I¹³¹ accumulation rate of thyroid and PBI¹³¹ content of plasma showed decrease, when administered 30 and 50 gamma daily for 30 days. In this case, higher doses of estradiol may have influence upon thyroid gland through pituito-adrenocortical axis, playing as a sort of stress, by increase both in adrenal weight and in functional activation of adrenal cortex.
After treatment with hexestrol (50 gamma daily) and α- (methoxyphenyl)-β,β-diphenylacrylonitrile (1mg daily) for 30 days, these artificial estrogens produced histological thyroid proliferation, but no significant change was observed in I¹³¹ distribution of plasma and thyroid.
When progesterone 1mg daily was given for 10 days, histological appearance as struma colloides was frequently observed in normal rats, but in all animals which were treated for 30 days, increase of thyroid weight and tendency to proliferation of follicular epithel were proved. In the latter group, higher value was obtained in I¹³¹ accumulation rate of thyroid gland and PBI¹³¹ content of plasma. Tendency to proliferation was more prominent when 5 mg of progesterone was injected daily for 27 days, whereas I¹³¹ uptake by thyroid gland and PBI¹³¹ content of plasma were rather decreased.
In normal rats, increase of thyroid weight and poliferation as struma parenchymatosa were produced by the injection of cortisone acetate (1.25-2.5 mg daily) and ACTH (4-10 mg daily) for 15-30 days, while I¹³¹ accumalation rate of thyroid and PBI¹³¹ content of plasma were constantly suppressed by treatment of cortisone acetate. As total I¹³¹ content of plasma also showed low value at 24 hours after injection of I¹³¹, the writer is inclined to accept the hypothesis of Berson and Ingbar et al that iodine deficiency of body is caused by the increased output from kidney, when cortisone acetate is used.
With dosage of 5 mg daily for 30 days, desoxycorticosterone acetate induced an increase in thyroid weight and a marked decrease in the uptake of I¹³¹ by the thyroid, but neither histological proliferation nor significant change in total I¹³¹ and PBI¹³¹ content of plasma observed.
Above mentioned follicular hormones (in higher doses), luteoid hormone and desoxycorticosterone acetate were given to hypophysectomized rat,

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