Kaoru Abe

Normal and abnormal regulation of β-MSH in man

A B S T R A C T The regulation of plasma 8-melanocyte-stimulating hormone (,8-MSH) in man has been studied utilizing a radioimmunoassay previously described (1). In normal subjects plasma p-MSH values ranged from 20 to 110 pg/ml. Metyrapone increased and dexamethasone decreased plasma P-MSH levels. Surgical stress stimulated f-MSH secretion. Plasma P-MSH levels were elevated in patients with untreated Addisons disease and untreated congenital adrenal hyperplasia, and these levels fell to normal during glucocorticoid therapy. In patients with Cushings syndrome due to pituitary adrenocorticotropic hormone (ACTH) excess, plasma fi-MSH was slightly elevated before treatment. In those patients who developed pituitary tumors and hyperpigmentation after bilateral adrenalectomy, plasma P-MSH was greatly elevated. In patients with Cushings syndrome due to adrenal tumor, plasma j9-MSH was subnormal. In patients with the ectopic ACTH syndrome, the levels of plasma f8-MSH were high. Plasma fi-MSH had a diurnal variation in normal subjects, patients with Addisons disease, and patients with congenital adrenal hyperplasia; but the normal diurnal variation was lost in patients with Cushings disease. In patients with high plasma 8-MSH, simultaneous determinations of plasma ACTH showed close correlation between the degree of elevation of ACTH and that of 8-MSH. In extracts of tumors from patients with the ectopic ACTH-MSH syndrome the quantities of the two hormones were roughly equivalent. In patients with hyperpigmentation due to a variety of disorders other than pituitary-adrenal abnormalities, plasma 8-MSH was normal. It is concluded that the secretion of P-MSH is regulated by the same factors that regulate ACTH.

Radioimmunoassay of β-MSH in Human Plasma and Tissues

: A radioimmunoassay method for beta-melanocyte-stimulating hormone (beta-MSH) has been developed and utilized in the identification and quantification of this hormone in human plasma and tissues. The concentration of beta-MSH in two human pituitary glands was found to be approximately 350 mug/g. beta-MSH was identified in the tumor tissue of all 11 patients with the ectopic ACTH syndrome who were studied; concentrations in individual cases ranged from 3 to 1600 ng/g. In plasma of chronically hyperpigmented patients with Addisons disease, Cushings disease (after bilateral adrenalectomy), and the ectopic ACTH syndrome, beta-MSH concentrations of 0.5-6 ng/ml were found. The degree of clinical hyperpigmentation was well correlated with the quantity of beta-MSH in the plasma. beta-MSH concentrations in the plasma of normal subjects were less than 0.09 ng/ml. In all of these circumstances, bioassays for MSH were also performed, and it was found that most of the biologic MSH activity of the plasma and tissues could be accounted for by beta-MSH.

ACTH Antibodies in Patients Receiving Depot Porcine ACTH to Hasten Recovery from Pituitary-Adrenal Suppression*

Six patients who had experienced prolonged steroid-induced pituitary-adrenal suppression were treated with 100 U of depot procine ACTH every 2 to 4 days for several months. Such treatment did not hasten the recovery of normal pituitary-adrenal function compared with the rate of recovery of a group of similarly suppressed patients who received no depot ACTH. Eight of nine patients who received prolonged courses of depot porcine ACTH developed antibodies to ACTH that cross-reacted with endogenous ACTH, binding it in the circulation in inactive form and retarding its removal from the circulation. The presence of such antibodies did not in itself grossly alter pituitary-adrenal interrelationships.

[8] Bioassay of pigmentary hormones

Publisher Summary Several methods based on migration of melanin granules within amphibian melanophores are currently available for the bioassay of hormones affecting pigmentation. These hormones, which include the MSHs (melanoeyte stimulating hormone) and ACTHs (adrenoeortieotropie hormone), cause the melanin granules to disperse that results in darkening of the skin and a consequent decrease in reflection of incident light by the darkened skin. This decrease in reflection of incident light by the darkened skin forms the basis for the bioassay of pigmentary hormones as developed by Shizume et al. utilizing the isolated skin of the frog. This method is designed so that the reference standard and unknown are compared under identical conditions, the biologic response and its variation are objectively quantitated, and finally, the plan of the assay permits the use of dose-response lines.