O. H. Gaebler

UTILIZATION OF GLYCINE NITROGEN AT VARIOUS LEVELS OF GLYCINE INTAKE.

Metabolism of approximately 20 mg of N15from glycine, ingested as a single dose, was studied in each of 2 dogs, in 5 successive experiments wherein total intake of free glycine increased stepwise from 1.5 to 19.5 g/day. Output of N15 as total nitrogen, urea, and ammonia, as well as the amount in fibrinogen, were deter mined 6, 12, 24, and 48 hours after ingestion. Percentage of Nls retained after 24 hours, and the percentage observed in fibrinogen, were both inversely proportional to the logarithms of total free glycine intake. The 13-fold increase in glycine intake re duced the former percentage by about one third, and the latter by about two thirds. Rate of urea formation, expressed as milligrams of urea nitrogen per kilogram of body weight per hour, was a linear function of glycine intake during the most active period of catabolism (second 6-hour period after ingestion). Percentage of urinary ammonia originating from ingested glycine during the first two 6-hour periods increased linearly with glycine intake during the first 4 levels of supplementation, but not at the highest level. Glycine evidently had a sparing effect on formation of ammonia from other sources, but this effect was limited.

Diabetogenic Effects of Growth Hormone: The Role of the Adrenals in Nitrogen Loss

Houssay and Penhos cite numerous studies in which anterior pituitary preparations produced diabetogenic effects in the absence of the adrenals. In hypophysectomized, adrenalectomized, partially depancreatized dogs, they observed large increases in blood sugar after somatotropin or prolactin administration, and small increases after corticotropin. Hydrocortisone also produced diabetic hyperglycemia in their animals. Early studies by Gaebler and Robinson support the contention of Houssay and Penhos that adrenalectomy does not abolish diabetogenic effects of growth hormone. Table 6 of the paper cited includes two experiments in which crude growth hormone was given to a dog with pancreas, adrenals, thyroid, and parathyroids removed. Lipemia, hyperglycemia, and increase in glucosuria all occurred in the first of these experiments, while in the second there was some increase in blood sugar. None the less, there was no loss of nitrogen, such as growth hormone elicited in depancreatized dogs with adrenals intact; in fact, some storage of nitrogen was induced in one of the two depancreatized-adrenalectomized animals, and both of them tolerated the growth hormone preparation much better than depancreatized ones. Thus the alleviating effects of adrenalectomy, so well established by Long and Lukens in cats/ and by Long in rats, were again confirmed in dogs. In the present study, we have investigated the nitrogen storing action and diabetogenic effect of a growth hormone preparation that is virtually free of corticotropin, and contains far less thyrotropic hormone than previous preparations. We have also attempted to reproduce the diabetogenic effects of growth hormone with corticotropin and hydrocortisone under our experimental conditions, and have carried out experiments to determine whether prolonged pretreatment of depancreatized dogs with hydrocortisone mitigates effects of growth hormone in a manner analogous to that observed by de Bodo and associates in hypophysectomized dogs.