Acetate: inhibitor of growth hormone hypersecretion in diabetic and non-diabetic uraemic subjects

1982 ◽  
Vol 99 (4) ◽  
pp. 551-558 ◽  
Author(s):  
Hans Ørskov ◽  
Aage Prange Hansen ◽  
Hans Erik Hansen ◽  
K. George M. M. Alberti ◽  
George A. Noy ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Normal Values ◽  
Hormone Secretion ◽  
Plasma Concentrations ◽  
Growth Hormone Secretion ◽  
Hormone Release ◽  
Plasma Growth Hormone ◽  
Blood Samples ◽  
Hormone Levels

Abstract. Five diabetic and 14 non-diabetic uraemic patients on long-term haemodialysis were studied during twenty-one 24 h periods including 5 to 7 h of haemodialysis against glucose-free acetate buffered dialysis fluid. Half-hourly blood samples were collected for hormonal and metabolite analysis. In addition, blood samples were analyzed in 40 experiments covering the haemodialysis and a pre-dialysis period. Before dialysis, plasma growth hormone levels were high and fluctuating, but almost always fell to low normal values within the first 2 h of haemodialysis. In the diabetic uraemic patients, the occasional severe hypoglycaemic episodes occurring during haemodialysis did not provoke growth hormone release, and hypoglycaemic reactions were not encountered. Intravenous acetate infusion studies resulted in plasma concentrations ranging from 1.3 to 2.7 mmol, i.e. about 60 per cent of the levels reached during haemodialysis and in suppression of growth hormone secretion. It is suggested that the fall in growth hormone levels and the lack of hypoglycaemic symptoms during haemodialysis is due to the use of acetate as a fuel in brain.

DIFFERENT EFFECTS OF EXOGENOUS CYCLIC ADENOSINE MONOPHOSPHATE AND ITS DIBUTYRYL DERIVATIVE ON PLASMA GROWTH HORMONE, GLUCOSE, INSULIN AND CORTISOL

1976 ◽  
Vol 83 (1) ◽  
pp. 15-25
Author(s):  
M. Vanderschueren-Lodeweyckx ◽  
W. Proesmans ◽  
E. Eggermont ◽  
R. Eeckels
Keyword(s):  
Growth Hormone ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Normal Subjects ◽  
Immunoreactive Insulin ◽  
Plasma Growth Hormone ◽  
Hormone Levels ◽  
The Mean

ABSTRACT The effects of the infusion in four different dosages (0.001, 0.005, 0.02 and 0.2 mg/kg/min during 60 min) of cyclic 3′,5′-adenosine monophosphate and of its dibutyryl derivative on plasma growth hormone and on glucose, immunoreactive insulin and cortisol were studied in 38 normal subjects and in 10 patients with idiopathic hypopituitarism. In normal subjects cyclic 3′,5′-adenosine monophosphate provokes an increase in plasma growth hormone levels (only when a dosage of 0.2 mg/kg/min is used) without any changes in plasma glucose, insulin and cortisol. The maximal value of the means is observed 75 min after starting the infusion. Dibutyryl cyclic 3′,5′-adenosine monophosphate (0.2 and 0.02 mg/kg/min) provokes a dose-related rise in plasma growth hormone levels which is always preceded by hyperglycaemia and hyperinsulinaemia. The peak of the mean growth hormone levels occurs at 135 min after initiation of the infusion. In all but one hypopituitary patients the nucleotides do not promote growth hormone secretion. It is concluded that exogenous cyclic 3′,5′-adenosine monophosphate and its dibutyryl derivative may not be considered as analogous and that both compounds may contribute to study growth hormone release in normal subjects and in patients with growth abnormalities.

LONG-TERM TREATMENT OF ACROMEGALY WITH BROMOCRIPTINE

1978 ◽  
Vol 87 (4) ◽  
pp. 687-700 ◽  
Author(s):  
Peter Claes Eskildsen ◽  
Per Aaby Svendsen ◽  
Lisbeth Vang ◽  
Jørn Nerup
Keyword(s):  
Growth Hormone ◽  
Hormone Secretion ◽  
Visual Fields ◽  
Growth Hormone Secretion ◽  
Term Treatment ◽  
Prolactin Secretion ◽  
Plasma Growth Hormone ◽  
Free Cortisol ◽  
Long Term Treatment

ABSTRACT Treatment with bromocriptine, 30–55 mg daily, in 13 acromegalics for 1–15 months, resulted in a 60 % decrease in growth hormone secretion, as judged from the excretion of growth hormone in 24-h urine. Normal excretion was obtained in 10 patients, while 1 patient showed no response. The plasma growth hormone response to O-GTT was improved, but not normalized, in 4 of 7 patients treated for more than 6 months, and marked glucosuria disappeared in two diabetics. While the secretion of TSH, LH and FSH was unchanged, the prolactin secretion was inhibited. The urine excretion of free cortisol showed a 30 % decrease, possibly due to a direct effect of bromocriptine on the ACTH-secretion. Hypercalcaemia was never seen, but the initial hypercalcuria showed a modest decrease without measurable changes in the creatinine clearance. The subjective relief during long-term treatment was marked in 10 of 11 patients and the dominating symptoms disappeared in 40–67 %, whereas heal-pad thickness, enlarged sellae, and visual fields remained unchanged. No serious side effects were observed. Treatment with bromocriptine seems effective and should be considered as a remedy amongst others, in suitable cases of acromegaly.

Effect of epoxyeicosatrienoic acids on growth hormone release from somatotrophs

1989 ◽  
Vol 256 (2) ◽  
pp. E221-E226 ◽  
Author(s):  
G. D. Snyder ◽  
P. Yadagiri ◽  
J. R. Falck
Keyword(s):  
Growth Hormone ◽  
Arachidonic Acid ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Epoxyeicosatrienoic Acids ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Growth Hormone Releasing Hormone ◽  
Epoxyeicosatrienoic Acid ◽  
Releasing Hormone

Growth hormone secretion was stimulated in vitro by products of arachidonic acid epoxygenase, the epoxyeicosatrienoic acids. 5,6-Epoxyeicosatrienoic and 14,15-epoxyeicosatrienoic acid stimulated growth hormone release from an enriched population of somatotrophs (approximately 85%) by twofold. Inhibition of arachidonic acid metabolism by indomethacin did not affect growth hormone-releasing hormone stimulation of growth hormone release. In contrast, pretreatment of somatotrophs with an 11,12-isonitrile analogue of arachidonic acid that inhibits arachidonic acid epoxygenase, resulted in a 20-25% inhibition of growth hormone-releasing hormone-stimulated growth hormone release. 14,15-Epoxyeicosatrienoic acid stimulated a concentration-dependent increase (twofold) in the cytoplasmic concentration of adenosine 3',5'-cyclic monophosphate (cAMP) in the somatotrophs. 14,15-Epoxyeicosatrienoic acid also rapidly increased the intracellular free calcium concentration in somatotrophs from resting levels (approximately 80 nM) to greater than 250 nM. Growth hormone-releasing hormone increased the free intracellular calcium to 160-180 nM. Preincubation of somatotrophs with somatostatin inhibited growth hormone-releasing hormone-stimulated growth hormone secretion, cAMP accumulation, and 14,15-epoxyeicosatrienoic acid stimulated cAMP accumulation. These data are suggestive that the epoxyeicosatrienoic acids may have a role in the secretion of growth hormone.

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