Growth Hormone Phosphorus

Renal elimination of phosphorus is regulated by PTH, calcitriol, growth hormone, insulin, and insulin-like growth factors. While the above-mentioned hormones show a number of other effects, the existence of a hormone affecting selectively the extracellular concentration of phosphorus is expected. The task of this hormone with phosphaturic effect has been speculated about from the beginning of the 1990s. It was named phosphatonin, and its increased concentration is found especially in patients with osteomalacia (tumor-induced osteomalacia, X-linked hypophosphatemic rickets, epidermal nevus). The phosphaturic effect of... 

Although the CYP27B1 gene is only 5 kb in size, the regulation is quite complex. The promoter is in the — S5/+22 region and requires a functional CCATT element. Three consensus AP-1 sites are upstream . Enzyme activity has long been known to be stimulated by low phosphorus diets (in animal models) " , and more recently, this phenomenon has been linked to a growth hormone mechanism " its relevance in humans is not known. 

Effect on Electrolytes. The administration of human growth hormone raises the intracellular levels of electrolytes, leads to a loss of bone calcium, and reduces urinary levels of phosphorus, potassium, and sodium. The increase in intracellular electrolytes may result from an increase in the cellular mass. Mobilization of bone calcium leads to osteoporosis in acromegaly and calciuria. Two explanations offered for this are (1) increased glomerular filtration combined with inhibition of tubular reabsorption, and (2) stimulation of parathyroid secretion. 

There is no satisfactory explanation for the reduced levels of phosphorus, potassium, and sodium found in urine of individuals injected with growth hormone. The hormone is believed to stimulate glomerular filtration at the same time that it increases tubular reabsorption. Although the reasons for increased reabsorption of potassium and sodium are obscure, it is possible to speculate on the reasons for phosphorus reabsorption. Increased tubular reabsorption of phosphorus is not accompanied by increased levels of phosphorus in the blood, and therefore phosphorus could be concentrated in the tissue where it stimulates growth. 

Mechanism of Action A polypeptide hormone that stimulates cartilaginous growth areas of long bones, increases the number and size of skeletal muscle cells, influences the size of organs, and increases RBC mass by stimulating erythropoietin. Influences the metabolism of carbohydrates (decreases insulin sensitivity), fats (mobilizes fatty acids), minerals (retains phosphorus, sodium, potassium by promotion of cell growth), and proteins (increases protein synthesis). Therapeutic Effect Stimulates growth. 

Conversion of 7-dehydrocholesterol to vitamin D3 and metabolism of D3 to l,25(OH)2D3 and 24,25(OH)2D3. Control of the latter step is exerted primarily at the level of the kidney, where low serum phosphorus, low serum calcium, and high parathyroid hormone favor the production of l,25(OH)2D3, whereas fibroblast growth factor 23 inhibits its production. The inset shows the... 

Previous diagnostic evaluation had included an electroencephalogram, brain scan, and chromosomal studies, which were unremarkable. Also normal were the plasma levels of electrolytes, calcium, phosphorus, magnesium, bilirubin, thyroxine, thyroid-stimulating hormone, and growth... 

It has been clearly demonstrated that the Krebs cycle functions in bone. Thus, in normal bone, oxaloacetate and pyruvate are converted to citrate, which is rapidly oxidized. Citrate accumulates under the influence of the parathyroid hormone without increasing its rate of oxidation. In contrast, estrogens accelerate both citric production and citrate oxidation. However, these phenomena may be several steps removed from the primary mechanism triggering phosphorus and calcium fixation on bone tissue, in view of the fact that no correlation between Krebs cycle activity and the uptake of phosphorus and calcium from the medium has been established. Thus, this effect of the hormones on the Krebs cycle may simply reflect hormonal stimulation of growth and protein synthesis in those tissues. 

Because of the possibility of its biosynthesis in the body and its biological function (it is an antirachitic vitamin connected with the metabolism of calcium and phosphorus, which are necessary for growth, development and maintenance of bone structure), some reports state that vitamin Dj is more a hormone than a vitamin. 

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