Peptide hormones, some new developments and their clinical implications

Engel, Frank L.; Lebovitz, Harold E.

doi:10.1016/0002-9343(63)90235-3

Cited by 83 publications

(1 citation statement)

References 32 publications

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“…In addition, we considered the possibility that the MSH could stimulate other processes besides glucocorticoid production in the fetal glands. In the adult adrenal cortex, ACTH stimulates not only steroidogenesis, but also the synthesis of DNA, RNA, and protein,2 the breakdown of glycogen, and the oxidation of glucose (9)(10)(11)(12). Accordingly, we measured the effect of ACTH, aMSH, and 3MSH on the incorporation by fetal adrenals of thymidine and leucine into DNA and protein, respectively.…”

Section: Introductionmentioning

confidence: 99%

Effects of melanotropic peptides on fetal adrenal gland.

Rudman¹,

Hollins²,

Lewis³

et al. 1980

J. Clin. Invest.

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A B S T R A C T Adrenal glands from early, mid, and late fetuses of rabbit, guinea pig, and rat, and from newborn animals of each species, were incubated for 1-4 h with and without 0.1 nM-1 ,uM ACTH, a-or ,B-melanocyte-stimulating hormone (aMSH or ,3MSH).The effects of the peptides were measured on production of glucocorticoids, and on incorporation of labeled thymidine or leucine into DNA or protein, respectively. The findings were similar in all three species. ACTH stimulated synthesis of glucocorticoids throughout fetal life. Potency increased progressively, as reflected by declining minimal effective dose and rising maximal response. In early and mid fetus aMSH and fMSH caused a modest glucocorticoid steroidogenic effect. ACTH and aMSH stimulated DNA and protein synthesis in the early and mid fetal gland. aMSH was more potent than ACTH in these respects, minimal effective dose being generally 10 times less and maximal response 25-200% greater. The effects diminished or disappeared in the late fetal and newborn gland. These data indicate that a-and 8M SH possess steroidogenic or growth-promoting properties, or both, for the fetal adrenal gland.

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Section: Introductionmentioning

confidence: 99%

Effects of melanotropic peptides on fetal adrenal gland.

Rudman¹,

Hollins²,

Lewis³

et al. 1980

J. Clin. Invest.

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Studies in Hypoglycemia of Infancy and Childhood

Antony¹,

Underwood²,

Wyk³

et al. 1967

Am J Dis Child

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ALTHOUGH elaborate classifications have been proposed, most children who develop hypoglycemia after the newborn period still fall into the group vaguely termed "idiopathic hypoglycemia of infancy and childhood." This study was undertaken to determine whether the clinical features and the responses to standard tests of blood sugar regulation are sufficiently distinctive to discriminate "idiopathic" cases from those of known etiology or provide any clues to possible etiologic mechanisms within the idiopathic group. This was done by analyzing the findings in a group of infants and children with idiopathic hypoglycemia and contrasting them with those in selected cases of hypoglycemia caused by hypopituitarism or insulinoma.A further objective of this study was to resolve some of the conflicting recommendations for the management of these patients. This report is based on the records of selected children admitted with the diagnosis of hypoglycemia to the North Carolina Memorial Hospital and Vanderbilt University Hospital. Much of these data were obtained under the ordinary pediatrie ward conditions of the two teaching hospitals. These retrospective analyses are reported together with the results of controlled therapeutic trials performed at the Clinical Research Unit of the North Carolina Memorial Hospital. Materials and Methods Clinical Data.-The charts of children admitted for hypoglycémie convulsions at North Carolina Memorial Hospital and Vanderbilt UniversityHospital were reviewed. Only those patients whose convulsions were proven on one or more occasions to be due to hypoglycemia at a time when no other illness was evident were included in the analysis. Patients were excluded if their hypoglycémie episodes were limited to the neo¬ natal period, or if, on further study, they were found to have glycogen storage disease, galac¬ tosemia, hypopituitarism, liver disease, episodic ketosis, or some other systemic illness. Other patients were not included because their data were insufficient to rule out these disorders or to contribute meaningful information. Thirteen infants and children met these criteria and were selected for analysis. Their findings were con¬ trasted with those of five other patients who were first admitted because of hypoglycémie seizures, but in whom the cause of the hypo¬ glycemia was eventually proven to be hypo¬ pituitarism or an insulinoma. The patients were grouped as follows: Group 1.-This group contained seven infants with hypoglycemia of undetermined cause with the onset of symptoms before 1 year of age. Group 2.-This group contained six children with hypoglycemia of undetermined cause with the onset of symptoms after 1 year of age. Group 3.-Three children with documented

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Bronchogenic carcinoma simulating hyperparathyroidism

Turkington

Goldman

Ruffner

et al. 1966

Cancer

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Four cases are reported of hypercalcemia and bronchogenic carcinoma without demonstrable bone metastases. Studies on serum calcium and phosphorous, phosphate clearance, urinary calcium, rapid calcium infusion test, and ultrafiltrable serum calcium indicated changes characteristic of primary hyperparathyroidism. Surgical extirpation of the lung carcinoma in 2 cases reverted these parameters to normal while x‐radiation of the other 2 carcinomas transiently returned serum calcium and phosphorus to normal levels. Adrenocorticoid therapy caused partial suppression of hypercalcemia in 2 instances. All 4 tumors were squamous cell carcinomas. It is concluded that the single criterion for establishing that hypercalcemia is secondary to a humorally active nonmetastatic tumor is the reduction of serum calcium in response to x‐radiation or surgical removal of the tumor.

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Peptide hormones, some new developments and their clinical implications

Cited by 83 publications

References 32 publications

Effects of melanotropic peptides on fetal adrenal gland.

Effects of melanotropic peptides on fetal adrenal gland.

Studies in Hypoglycemia of Infancy and Childhood

Bronchogenic carcinoma simulating hyperparathyroidism

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