Regulation of Growth Hormone Secretion in Man: A Review

Johnston, Desmond G.; Davies, R.R.; Prescott, R. W. G.

doi:10.1177/014107688507800410

Cited by 24 publications

(12 citation statements)

References 44 publications

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“…Interest in growth hormone (GH) in diabetes centres on its anti-insulin effects and its possible role in the long-term complications of the disease (1). Growth hormone, along with glucagon, cortisol, and the catecholamines, has effects on glucose metabolism and ketosis which are antagonistic to those of insulin.…”

Section: Growth Hormone In Diabetesmentioning

confidence: 99%

Effects of Somatostatin and SMS 201-995 on Carbohydrate Metabolism in Normal Man

Johnston

Davies

Turner

1986

Scandinavian Journal of Gastroenterology

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Johnston DG, Davies RR, Turner SJ. Effects of somatostatin and SMS 201-995 on carbohydrate metabolism in normal man. Scand J Gastroenteroll986,21 (suppl119), Growth hormone (GH) is important in diabetes in view of its anti-insulin actions and its relation to the long-term complications of the disease. The suppression of G H secretion in diabetics has theoretical and possible therapeutic interest. Native somatostatin has multiple actions, including inhibition of the secretion of insulin, glucagon, thyroid-stimulating hormone (TSH), and various gut hormones. It also has inhibitory effects on gastrointestinal motility, exocrine secretion, nutrient absorption, and splanchnic blood flow. Its therapeutic use is limited by a duration of effect of several minutes only. SMS 201-995 holds more potential than native somatostatin in view of its longer duration of action. Preliminary data suggest that 50pg SMS 201-995 subcutaneously at night inhibits the noctural rise in GH secretion in normal man, hut no effect on 24-h G H secretion is observed when SMS 201-995 is injected twice daily before meals. SMS 201-995 inhibits secretion of insulin. glucagon, and TSH in addition to growth hormone and induces carbohydrate intolerance when administered before food in normal subjects. Gastrointestinal side effects suggest additional effects on nutrient disposal, which are important when it is administered before food. Further studies are required to elucidate these effects of SMS 201-995 on endocrine and gastro-intestinal function in normal and diabetic man. upon Tyne NE2 4HH, U K 158-1 65.Scand J Gastroenterol Downloaded from informahealthcare.com by QUT Queensland University of Tech on 11/02/14For personal use only.Scand J Gastroenterol Downloaded from informahealthcare.com by QUT Queensland University of Tech on 11/02/14For personal use only.

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Section: Growth Hormone In Diabetesmentioning

confidence: 99%

Effects of Somatostatin and SMS 201-995 on Carbohydrate Metabolism in Normal Man

Johnston

Davies

Turner

1986

Scandinavian Journal of Gastroenterology

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“…The bulk of GH release is observed at the onset of slow-wave sleep and at more unpredictable secretory episodes a few hours following meals [1][2][3], During fast ing and during various conditions of stress GH secre tion is increased [3,4], whereas excess of fuels such as glucose and lipid intermediates inhibits GH release [4], These observations evidently suggest that the biological effects of GH may predominantly be exerted during states of relative fuel shortage, such as fasting or pro longed exercise. A normally proportioned 70-kg man has access to 300-400 g glycogen (1.500 kcal), 6-7 kg mobilizable muscle protein (25,000 kcal) and 10-15 kg triacylglycerol in adipose tissue (125,000 kcal) [5].…”

Section: Introductionmentioning

confidence: 99%

Effects of Growth Hormone on Glucose Metabolism

et al. 1991

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Growth hormone (GH) counteracts in general the effects of insulin on glucose and lipid metabolism, but shares protein anabolic properties with insulin. Under physiological circumstances GH does not affect total glucose turnover directly. There is however evidence that GH acutely decreases glucose oxidation (secondary to an increase in lipid oxidation) and suppresses muscle uptake of glucose, suggesting that GH redistributes glucose fluxes into a non-oxidative pathway, which could be a build up of glycogen depots through gluconeogenesis. Since GH secretion is inhibited in the fed state these actions are mainly important in the postprandial or fasting state. Under pathological conditions of GH excess (e.g. acromegaly, poorly controlled tp. 1 diabetes or high dose GH treatment) the diabetogenic actions of GH become apparent. In these patients increased endogenous glucose production, decreased muscle glucose uptake and rising blood glucose levels are observed. In patients with intact β-cell function these changes are counterbalanced by hyperinsulinemia – such hyperinsulinemia may in the long term induce increased cardiovascular morbidity and mortality (‘Reavens syndrome X’). When stimulated with insulin these patients exhibit insulin resistance at the liver, in adipose tissue and in muscle. Few elaborate studies on the effects of GH on glucose metabolism in GH deficient patients have been conducted. These patients are hypersensitive to the actions of insulin on glucose metabolism and there is some evidence that when GH initially is given to such patients in the GH deprived state, paradox insulin-like effects of GH may be observed. Whether this may relate to increased activity of insulin-like growth factors is unsettled.

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“…Our findings support the hypothesis that G R F and insulin-induced hypoglycaemia release GH via different pathways which are, at least in part, additive.GH secretion from the anterior pituitary (AP) gland is controlled by the inhibitory peptide somatostatin and the releasing peptide G R F (Wass, 1983; Guilleman et al, 1984;Johnston et al, 1985). Peak GH responses to separate administration of insulin and G R F were comparable (71.4 rf: 10.2 vs 70.1 f 27.7 mU/l; mean f SEM).…”

mentioning

confidence: 99%

“…GH secretion from the anterior pituitary (AP) gland is controlled by the inhibitory peptide somatostatin and the releasing peptide G R F (Wass, 1983; Guilleman et al, 1984;Johnston et al, 1985). Pituitary G H reserve can be assessed using several metabolic and neuropharmacological tests of which the commonest are insulin-induced hypoglycaemia…”

mentioning

confidence: 99%

Additive Effects of Growth Hormone Releasing Factor and Insulin Hypoglycaemia on Growth Hormone Release in Man

Page

Koppeschaar

Edwards

et al. 1987

Clinical Endocrinology

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We have measured GH and PRL changes following separate and combined administration of insulin and GH releasing factor (GRF) in six normal males. Peak GH responses to separate administration of insulin and GRF were comparable (71.4 +/- 10.2 vs 70.1 +/- 27.7 mU/l; mean +/- SEM). However, the peak GH response following combined administration was significantly higher (120.8 +/- 29.7, P less than 0.05) as was the total GH released as calculated by measuring the area under the curve (P less than 0.05). In contrast the PRL response to hypoglycaemia was not altered by the combined administration of insulin and GRF. This effect was not due to any direct action of hypoglycaemia or insulin at pituitary level since basal and 10(-8) M GRF stimulated GH release from rat anterior pituitary cells in vitro was not influenced by varying glucose and insulin levels. Our findings support the hypothesis that GRF and insulin-induced hypoglycaemia release GH via different pathways which are, at least in part, additive.

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Regulation of Growth Hormone Secretion in Man: A Review

Cited by 24 publications

References 44 publications

Effects of Somatostatin and SMS 201-995 on Carbohydrate Metabolism in Normal Man

Effects of Somatostatin and SMS 201-995 on Carbohydrate Metabolism in Normal Man

Effects of Growth Hormone on Glucose Metabolism

Additive Effects of Growth Hormone Releasing Factor and Insulin Hypoglycaemia on Growth Hormone Release in Man

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