Hypothalamic Secretion of Somatostatin and Growth Hormone-Releasing Factor into the Hypophysial-Portal Circulation Is Reduced in Streptozotocin Diabetic Male Rats

1991 ◽  
Vol 53 (5) ◽  
pp. 433-438 ◽  
Author(s):  
Paul M. Plotsky
Endocrinology ◽  
1986 ◽  
Vol 118 (5) ◽  
pp. 2109-2114 ◽  
Author(s):  
GIAN PAOLO CEDA ◽  
GIORGIO VALENTI ◽  
UGO BUTTURINI ◽  
ANDREW R. HOFFMAN

1977 ◽  
Vol 86 (1) ◽  
pp. 71-80 ◽  
Author(s):  
Morton A. Vodian ◽  
Charles S. Nicoll

ABSTRACT Relationships between depletion of growth hormone (GH) from the rat adenohypophysis and its release into the circulation were re-evaluated using bioassay (BA: rat tibia test) and radioimmunoassay (RIA). Anaesthetized male rats were injected with a putative growth hormone releasing factor ("GRF") and killed 15 and 30 min later. For the assays, the plasma and adenohypophyses were pooled; the latter were separated into granule and cytosol fractions prior to assay. Fifteen minutes after "GRF" injection the BA recorded a 75 % depletion of GH from the granular fraction but the RIA measured a loss of only 13 %. By 30 min both assays recorded restoration of pituitary GH. Only slight changes occurred in the levels of BA- or RIA-detectable GH in the cytosol fractions. The massive depletion of bioassayable GH from the granule fraction was accompanied by a large increase (3.2 mU/ml) in the plasma concentration of BA-detectable hormone by 15 min. The slight depletion of RIA-detectable GH that occurred during this time was associated with a meagre increase (0.05 mU/ml) in the plasma level of immunoreactive GH. The plasma concentration of BA- and RIA-detectable GH did not change significantly between 15 and 30 min. Analysis of the relationship between depletion of GH from the pituitary and its release into the extrapituitary compartment disclosed that the BA recordings of these events were in excellent quantitative agreement but RIA measurements were not. The results confirm that biologically active GH can be depleted from and released by the adenohypophysis in vivo independently of RIA-detectable GH.


1996 ◽  
Vol 148 (2) ◽  
pp. 189-192 ◽  
Author(s):  
D Olchovsky ◽  
J F Bruno ◽  
M Berelowitz

Abstract Growth hormone-releasing factor (GRF) mRNA expression in male rats occurs predominantly in the hypothalamus (mainly in the arcuate nucleus), and among extraneural sites primarily in the testis. Hypothalamic GRF is the physiological tropic stimulus to growth hormone secretion. However, the role of GRF in the testis is unknown. We have shown previously that hypothalamic GRF mRNA expression is significantly reduced in streptozotocin (STZ)-diabetic rats. This reduction is confined to the arcuate nucleus and probably accounts for the suppression of growth hormone pulsatility. The present studies were performed to evaluate GRF expression in the testis of streptozotocin (STZ)-diabetic rats. Diabetes was induced by injection of STZ (100 mg/kg i.p.). Seventeen to twenty days later diabetic rats were hyperglycemic compared with vehicle-injected controls and demonstrated growth failure. Insulin treatment reduced the glycemia and increased body weight towards normal. Total RNA was extracted from the hypothalamus and testis, and GRF mRNA levels estimated by solution hybridization/nuclease protection assay. Levels of hypothalamic somatostatin mRNA were measured to serve as control values. GRF mRNA was significantly (P<0·001) decreased in the hypothalamus of STZ-diabetic rats (0·2 ± 0·07 mean relative densitometric units, n=8) compared with controls (1·0 ± 0·19, n=8) with no change in somatostatin mRNA expression. In contrast, testicular GRF mRNA was increased 70% (P<0·05) in STZ-diabetic rats. Insulin treatment resulted in normalization of hypothalamic GRF mRNA levels (1·1 ± 0·17, n=5) with no effect on testicular GRF mRNA expression. In conclusion GRF gene expression is discordantly regulated in tissues of male STZ-diabetic rats. While reduced GRF expression may account for the low growth hormone state in this model, increased testicular GRF mRNA (with the previously reported reduction of insulin-like growth factor-I mRNA) resembles the response seen in growth hormone-sensitive tissue (especially the hypothalamus) to this growth hormone-deficient state. Journal of Endocrinology (1996) 148, 189–192


1985 ◽  
Vol 110 (1_Suppla) ◽  
pp. S144-S145
Author(s):  
M. LOSA ◽  
J. SCHOPOHL ◽  
P. G. CHIODINI ◽  
A. LIUZZI ◽  
K. VON WERDER

Diabetes ◽  
1986 ◽  
Vol 35 (1) ◽  
pp. 119-123 ◽  
Author(s):  
K. Hermansen ◽  
A. M. Kappelgaard ◽  
J. Esmann ◽  
H. Orskov

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