/pdf/insulin-i131-metabolism-in-human-subjects-demonstration-of-2dqbkiapju.pdf

Insulin-i131 metabolism in human subjects: demonstration of insulin binding globulin in the circulation of insulin treated subjects

https://cancerres.aacrjournals.org/content/canres/18/10/1118.full.pdf

The control of cell division: a review. II. Special mechanisms.

Although the pubertal surge of estrogen is the immediate stimulus to mammary development, the action of estrogen depends upon the presence of pituitary growth hormone and the ability of GH to stimulate production of IGF-I in the mammary gland. Growth hormone binds to its receptor in the mammary fat pad, after which production of IGF-I mRNA and IGF-I protein occurs. It is likely that IGF-I then works through paracrine means to stimulate formation of TEBs, which then form ducts by bifurcating or trifurcating and extending through the mammary fat pad. By the time pubertal development is complete a tree-like structure of branching ducts fills the rodent mammary fat pad. In addition to requiring IGF-I in order to act, estradiol also directly synergizes with IGF-I to enhance formation of TEBs and ductal morphogenesis. Together they increase IRS-1 phosphorylation and cell proliferation, and inhibit apoptosis. In fact, the entire process of ductal morphogenesis, in oophorectomized IGF-I(−/−) knockout female mice, can occur as a result of the combined actions of estradiol and IGF-I. IGF-I also permits progesterone action in the mammary gland. Together they have been shown to stimulate a form of ductal morphogenesis, which is anatomically different from the kind induced by IGF-I and estradiol. Although both progesterone and estradiol synergize with IGF-I by increasing IGF-I action parameters, there must be other, as yet unknown mechanisms that account for the anatomical differences in the different forms of ductal morphogenesis observed (hyperplasia in response to IGF-I plus estradiol and single layered ducts in response to IGF-I plus progesterone).

IGF-I, GH, and sex steroid effects in normal mammary gland development.

The renotropic and metabolic effects of human growth hormone were studied in 2 patients with hypopituitarism, 1 with cirrhosis of the liver and 2 with chronic nephritis and usemia. The dosage was 5 to 10 mg. a day for three to nine days. The plasma urea level and urea excretion decreased promptly in all subjects. The blood phosphorus and glucose levels increased gradually, and phosphorus excretion decreased. A renotropic effect was shown by the prompt increases in endogenous creatinine clearance and in phosphorus reabsorption. In the patient with cirrhosis of the liver who had hypocholesterolemia and hypoalbuminemia, the serum cholesterol and albumin levels increased, suggesting that liver function was stimulated. These results emphasize the important role of the growth hormone in adult man, and suggest its use as a therapeutic agent in certain diseased states.

Metabolic and renotropic effects of human growth hormone in disease.

https://acsjournals.onlinelibrary.wiley.com/doi/pdf/10.1002/1097-0142%281955%298%3A2%3C271%3A%3AAID-CNCR2820080206%3E3.0.CO%3B2-3

The effects of pituitary and adrenal hormones on the growth of a transplanted mammary adenocarcinoma in C3H mice.

Growth and adrenocorticotropic hormones of anterior pituitary.

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Growth and adrenocorticotropic hormones of anterior pituitary.