Radioautographic Studies on the Localization of 125i-Labelled Human Luteinizing and Growth Hormone in Immature Male Rats

Kretser, D. M. De; Catt, K. J.; Burger, Henry; Smith, Graeme C.

doi:10.1677/joe.0.0430105

Cited by 69 publications

(14 citation statements)

References 12 publications

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“…This was confirmed with the immunoperoxidase technique. Although these findings have not been reported for PTH, localization of insulin (33)(34)(35), glucagon (36), growth hormone (37)(38)(39), luteinizing hormone, and follicle-stimulating hormone (40,41), human chorionic gonadotropin (42), and prolactin (43) (13), and our current data-showing that localization of 125I-labeled and unlabeled preparations are identical, indicate that the metabolism ofthe radioiodinated PTH used in these studies accurately reflects the metabolism of unlabeled hormone.…”

Section: Discussioncontrasting

confidence: 52%

Analysis of Parathyroid Hormone and Its Fragments in Rat Tissues

D'Amour¹,

Segre²,

Roth³

et al. 1979

J. Clin. Invest.

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A B S T R A C T After intravenous injection of [125LI]iodo-parathyroid hormone in the rat, uptake of the hormone was greatest in the liver and kidneys. Uptake was rapid, reaching a maximal concentration by 4 and 8 min, respectively. Extracts, prepared from both these organs at intervals soon after the injection of intact hormone, showed three main radioactive peaks when samples were subjected to gel filtration under proteindenaturing conditions. The first peak coeluted with intact hormone.The second eluted at a position corresponding to the carboxy-terminal fragments previously described in plasma, and the last eluted at the salt volume of the column. Microsequence analysis of the radioiodinated fragments, a method that has proved valuable for chemically defining the circulating fragments resulting from metabolism of injected hormone, showed that extracts of liver and kidney, prepared at 4 and 8 min after injection of the intact hormone, contained different fragments. The radioiodinated fragments in liver extracts were identical to those previously reported in the plasma of rats and dogs, fragments resulting principally from proteolysis between positions 33 and 34, and 36 and 37 of the intact hormone. Although the same fragments were also present in the kidneys, they constituted less than 15% of the amount present in the liver. More than 50% of the

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Section: Discussioncontrasting

confidence: 52%

Analysis of Parathyroid Hormone and Its Fragments in Rat Tissues

D'Amour¹,

Segre²,

Roth³

et al. 1979

J. Clin. Invest.

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“…This finding suggests decreased production and/or release of LH. Since the kidney is an important organ involved in biodegradation of LH [26], one would expect that the serum levels of LH in acute renal failure would be ele vated if its production is normal. The finding of normal serum levels of LH in our patients provides further sup port for its decreased production and/or release.…”

Section: Discussionmentioning

confidence: 99%

Disturbances in the Hypothalamic-Pituitary-Gonadal Axis in Male Patients with Acute Renal Failure

et al. 1984

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The function of the hypothalamic-pituitary-gonadal (HPG) axis was examined in 20 male patients with acute renal failure. During the oliguric phase of the disease, the serum concentrations of follicle stimulating hormone (FSH) and total and unbound testosterone were markedly reduced, those of prolactin were elevated while those of luteinizing hormone (LH) were normal. The serum concentrations of sex hormone binding globulin were normal. During the diuretic phase of the illness, the serum levels of FSH and testosterone remained low but those of prolactin fell towards normal. After recovery of renal function, the abnormalities in the serum concentrations of these hormones were reversed. The responses of LH and FSH to gonadotropin releasing hormone and of prolactin to thyrotropin releasing hormone were abnormal and became normal after recovery of renal function. The results demonstrate that: (1) abnormalities in HPG axis occur early in the course of acute renal failure; (2) many features of these derangements are similar to those seen in chronic renal failure, and (3) the alterations in the function of the HPG axis are reversible when renal function is restored. The data suggest that loss of renal function, uremia per se and/or a metabolic consequence of uremia such as secondary hyperparathyroidism are responsible for these derangements.

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“…Second, a 3-day course of GH replacement therapy causes a significant decrease in corticosterone secretion (toward the normal levels) without altering cortisol secretion. Although GH receptors are present in high concentrations in the adrenal cortex (13) and there is an accumulation of labeled GH in the adrenal when ['25-1] GH is administered to rats (14), a specific regulatory effect of GH on this tissue has not been previously recognized. Thus, these experiments demonstrate that G H has a significant effect on steroid production in the adrenal cortex.…”

Section: Discussiokmentioning

confidence: 99%