Folia Endocrinologica Japonica

The Relation of Vitamin B₆ to Insulin

Tadataka KOIDE

1962 Volume 38 Issue 1 Pages 4-30,1
Published: April 20, 1962
Released on J-STAGE: September 24, 2012

DOIhttps://doi.org/10.1507/endocrine1927.38.1_4

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It is generally known that there is some evidence suggesting an intimate relationship between vitamin B₆, and diabetes mellitus. But almost nothing is known regarding the relationship between the action of insulin and vitamin B₆. In my study on this subject, I obtained the following results.
1) The cause of the diabetic state in rats, being fed a diet over a 2-to 3-month period in which vitamin B₆ was eliminated, may be attributed to the disturbance of insulin utilization but not to the xanthurenic acid which is produced during the deficient period.
2) The diabetic state in rats, being fed a diet over a 9-month period, in which vitamin B₆, was restricted to doses only sufficient to sustain life, is due to a lack of insulin.
3) It is conceivable that, one of the many factors contributing to the disturbance of insulin utilization has some relation with vitamin B₆, or the vitamin B₆ enzyme, because the disturbance of insulin utilization in diabetic patients with a high plasma insulin level is often corrected by the use of PAL-PO₄. Furthermore, the use of pyridoxine for the disturbance of oxydative phosphorylation in diabetics is not effective, the only effective agent being PAL-PO₄, which is the co-enzyme of pyridoxine.
These results clearly evidenced the intimate relationship between vitamin B₆, and diabetes in man. In conclusion, it is not the purpose of this report to emphasize the significance of PAL-PO₄ for the treatment of some types of diabetes, but to assert that vitamin B₆ is an important key for the resolution of the etiology and pathological physiology of diabetes mellitus.

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Study of Urinary 17-ketosteroids in Hyperthyroidism and Hypothyroidism

Minoru TANDA

1962 Volume 38 Issue 1 Pages 31-51,1
Published: April 20, 1962
Released on J-STAGE: September 24, 2012

DOIhttps://doi.org/10.1507/endocrine1927.38.1_31

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In hyperthyroidism, urinary 17-ketosteroids are in the lower limit of the normal value or low, and 17-hydroxycorticosteroids are normal or slightly increased. These data are widely accepted but the cause of the dissociation of these data is based on conjecture.
The author tried to clarify this dissociation with hormonal examinations as follows : 1. Urinary 17-KS were measured by Holtorff-Koch and var. Masuda's method. 2. Microscale liquid column chromatography by Edwards and var. Ohno's method. 3. Urinary 17-OHCS were hydrolyzed by bacterial beta-glucuronidase and measured by Porter-Silber's reaction. 4. Plasma 17-OHCS by var. Silber-Porter's method. 5 Urinary gonadotropin by the mouse uterine weight method. 6. ACTH-test by I. V. dripping of 25 units of ACTH for 6 hrs., and GTP-test by I.M. injection three to five times a day of Gonagenforte (Gonadotropin protamin) every three days.
In hyperthyroidism, urinary 17-KS were almost in the lower limit of the normal value or low but 17-OHCS in urine and blood were normal. GTP in urine were more than normal, but the chromatography of urinary 17-KS disclosed decreased androgenic 17-KS in more than half of the cases. In androgenic, 17-KS androsterone increased and etiocholanolone decreased. ACTH-test revealed increased urinary 17-KS, 17-OHCS, and androgenic 17-KS with normal response, though plasma 17-OHCS responded poorly in some cases. Urinary 17-KS and 17-OHCS measured by GTP-test were in the range of daily variation, and androgenic 17-KS did not increase.
Urinary 17-KS returned almost to normal value, and chromatography showed almost normal pattern after treatment.
In hypothyroidism, urinary 17-KS and 17-OHCS decreased remarkably and 17-OHCS in blood were normal. Urinary GTP and androgenic fraction of urinary 17-KS were both low. In androgenic 17-KS androsterone decreased and etiocholanolone increased. These data were opposite of hyperthyroidism. After treatment, urinary 17-KS and 17-OHCS returned almost to normal level and androsterone increased.
From these data I presume that in hyperthyroidism, over-secreted thyroxin supresses the reactivity of the gonadal tissue and adrenal glands to GTP and so the response of the adrenal gland to GTP decreases as compared to the response to ACTH and these factors cause the decrease of urinary 17-KS especially of the androgenic fraction. I also presume that in hypothyroidism, because of the decreased removal rate of steroid, plasma 17-OHCS are normal but urinary 17-KS, 17-OHCS become low, and that the decrease of GTP causes less production of androgenic 17-KS.
Thyroxin effects to metabolic changes of androgenic 17-KS in the peripheral tissues mainly in liver, and so in hyperthyroidism androsterone increases and in hypothyroidism decreases.

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Studies on the Pathogenesis of Adrenal Regeneration Hypertension of the Rat

Shinpei MORIMOTO

1962 Volume 38 Issue 1 Pages 52-70,2
Published: April 20, 1962
Released on J-STAGE: September 24, 2012

DOIhttps://doi.org/10.1507/endocrine1927.38.1_52

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In order to clarify the pathogenesis of adrenal regeneration hypertension of the rat, the author investigated the metabolism of corticosteroids, water and electrolytes in adrenal-enucleated animals and the histological changes in their organs every week while hypertension persisted. The results were as follows :
1) Hypertension above 130 mmHg accompanied by cardiac enlargement and renal lesions developed 5 weeks after adrenal enucleation.
2) The regenerating adrenal was 126 per cent as heavy as a normal gland 5 weeks after the enucleation. Histologically, the glomerular zone appeared in the second week, but regeneration of the reticular zone was not observable even after 8 weeks.
3) Adrenal-regeneration-hypertension rats showed a marked decrease in plasma corticosterone, urinary formaldehydrogenic corticoids and reducing corticoids on the seventh day, the values being respectively 12, 15 and 10 per cent of the values in control animals, and a gradual regression thereafter to near normal values. On the other hand, restratoin of 17-ketosteroids lagged behind and showed only 53 per cent of the normal value 8 weeks after the enucleation.
4) The regenerating adrenal gland showed normal respose to ACTH administration.
5) The remaining kidney showed a marked compensatory hypertrophy within one week after the enucleation and its extractable renin content had a gradual decrease as hypertension advanced.
6) The daily consumption of 1 per cent saline drinking solution was significantly higher in the experimental rats than in the control rats 2 weeks after the enucleation.
7) Serum sodium and potassium levels increased within one week of the enucleation procedure and returned to the normal level 2 weeks after the enucleation.
8) Urinary excretion of water, sodium and potassium decreased during the first week, but after 2 weeks, exaggerated water diuresis and slight increase in sodium excretion were observed.
9) During adrenal regeneration there were no excessive amounts of aldosterone nor any significant imbalance in the steroid pattern, compared with control animals.
A tentative interpretation of most of the findings was presented.

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[title in Japanese]

1962 Volume 38 Issue 1 Pages 71-92
Published: April 20, 1962
Released on J-STAGE: September 24, 2012

DOIhttps://doi.org/10.1507/endocrine1927.38.1_71

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