Physiological role of somatostatin in the control of growth hormone and thyrotropin secretion

Ferland, Louise; Labrie, Fernand; Jobin, M.; Arimura, Akira; Schally, Andrew V.

doi:10.1016/0006-291x(76)90022-x

Cited by 269 publications

(93 citation statements)

References 18 publications

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“…The plasma G H concentration was found to be markedly depressed in the rats with ARC lesions in the present study, similar to that found in rats with electrical or chemical lesions of the ARC in previous reports (1 5,19). CSH is known to be a depletor of SRIF and its reduction of SRIF levels in the hypothalamus is dose-dependent (16,20,21 (22,23).…”

Section: Discussionsupporting

confidence: 91%

Effects of Somatostatin on the Growth Hormone‐Releasing Factor‐Induced Growth Hormone Secretion in Rats with Electrical and Chemical Inhibitions of Endogenous Growth Hormone‐Releasing Factor and Somatostatin

Sato

Takahara

Niimi

et al. 1990

J Neuroendocrinology

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The episodic pattern of growth hormone (GH) secretion of the male rat was simulated in rats exhibiting impaired GH-releasing factor (GRF) and somatostatin (SRIF) secretion, by administering various combinations of human GRF-(1-44)NH2 (hGRF) and SRIF. Electrical lesions of the arcuate nucleus resulted in a marked decrease in the amplitude of GH secretory bursts, while the administration of cysteamine (200 mglkg) did not change the GH secretory profile in rats with arcuate nucleus lesions. lmmunohistochemical examinations revealed a marked decrease of GRF and SRlF immunoreactivity in the median eminence of the cysteamine-treated rats with arcuate nucleus lesions. The intravenous injection of 5 pg of hGRF every 3 h caused equivalent surges of GH in the cysteamine-treated rats with arcuate nucleus lesions. The additional infusion of 4 pglh of SRlF during the trough periods of GH secretion did not affect the amplitude of the GH surges. Hourly injection of 5 pg of hGRF caused transient desensitization to hGRF. Interestingly, the additional infusion of 4 pglh of SRlF every 3 h enhanced the amplitude of the GH bursts induced by the fourth and the seventh hGRF injections. However, the more frequent injection of 5 pg of hGRF every 30 min caused constant desensitization to hGRF with time, and the additional infusion of 4 pglh of SRlF every 3 h did not change the attenuated responses to hGRF. These results indicated that the simultaneous administration of hourly GRF and continuous SRlF with brief pauses was most effective for producing high GH peaks. This simulation model suggests that SRlF may play an important role not only in the production of GH troughs, but also in the maintenance of GH surges with distinct peaks in the male rat.

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Section: Discussionsupporting

confidence: 91%

Effects of Somatostatin on the Growth Hormone‐Releasing Factor‐Induced Growth Hormone Secretion in Rats with Electrical and Chemical Inhibitions of Endogenous Growth Hormone‐Releasing Factor and Somatostatin

Sato

Takahara

Niimi

et al. 1990

J Neuroendocrinology

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“…Williams et al [29] also reported more potent inhibitory effect of SRIH on GH compared to TSH secretion in men. Other supporting evidence has been reported by several investigators, where treatment of animals with SRIF antiserum increases both GH and TSH levels [30][31][32]. However, more marked stimulatory effects of SRIH antiserum on GH compared to TSH levels were observed [31,32].…”

Section: Discussionsupporting

confidence: 73%

Acute Hyperglycemia and Activation of the .BETA.-Adrenergic System do not Exhibit Synergistic Inhibitory Actions on Thyrotropin-releasing Hormone (TRH)-induced Thyroid Stimulating Hormone (TSH) Secretion

et al. 2005

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Abstract. Thyrotropin-releasing hormone (TRH)-stimulated thyroid stimulating hormone (TSH) response in normal subjects is suppressed by oral glucose administration. Pharmacologic studies indicate that this suppressive action of glucose is mediated by an increase in hypothalamic somatostatin (SRIH) tone. Since activation of the b-adrenergic system also suppresses basal TSH secretion by enhancing SRIH release we sought to determine whether isoproterenol alters the suppression of TRH-induced TSH response induced by the stimulation of glucose. Four tests were performed in seven healthy young men: Test 1: 200 mg TRH (iv) at 0 min; Test 2: 100 g oral glucose at -30 min and TRH at 0 min; Test 3: TRH at 0 min with isoproterenol (0.012 mg/kg, iv) infused continuously; Test 4: oral glucose at -30 min, TRH at 0 min with isoproterenol infused continuously. Pretreatment with glucose significantly suppressed TRH-induced TSH secretion. Isoproterenol infusion also suppressed the TRH-induced TSH secretion, but it did not enhance the inhibitory action of glucose on TSH secretion. The degree of suppression induced by glucose was significantly higher than that achieved by isoproterenol. These data suggest that combined administration of glucose and isoproterenol does not exhibit synergistic inhibitory actions on TRH-stimulated TSH secretion, and that the glucose-TRH test could be used for the evaluation of the hypothalamic somatostatinergic activity.Key words: Hyperglycemia, Isoproterenol, Thyrotropin-Releasing Hormone (TRH), Thyroid Stimulating Hormone (TSH) (Endocrine Journal 52: 69-74, 2005) NO direct method is yet available to measure the hypothalamic somatostatinergic activity in humans. As alternatives, various pharmacological agents have been used to estimate central somatostatin (SRIH) tone indirectly. Many studies have utilized agents that suppress SRIH release; these include arginine [1, 2], propranolol [3], and pyridostigmine [2,4]. On the other hand, several studies have used agents thought to enhance SRIH release which include acute hyperglycemia [5,6] and b-adrenergic agonists [7][8][9]. Our laboratory, as well as others, has observed that both of these stimuli block GHRH-induced GH release [10][11][12][13]. Recently we have reported that the degree of suppression of the GH response to GHRH, initiated by glucose and the badrenergic agonist, isoproterenol, was comparable, while the combined effects were significantly higher than that achieved by glucose and isoproterenol alone [10]. In addition, propranolol, a b-adrenergic antagonist was not able to block glucose-induced suppression of GHRH-stimulated GH release. These results sug-

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“…In addition to its endocrine role in the hypothalamus, i.e. inhibition of the release of growth hormone and to some extent also of thyrotropin from the anterior pituitary [17], there is strong evidence for paracrine functions of somatostatin in the gastroenteropancreatic system [18], where it inhibits the secretion of insulin and glucagon from the pancreas. It was also found that somatostatin inhibits the secretions of gastrin, motilin and other gastrointestinal hormones [ 191.…”

Section: Discussionmentioning

confidence: 99%

Immunoreactive and biologically active somatostatin in human and sheep milk

Werner

Amarant

Millar

et al. 1985

European Journal of Biochemistry

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The presence of immunoreactive and biologically active somatostatin in sheep and human milk has been demonstrated. Milk somatostatin exhibits similar chromatographic behavior to that of synthetic somatostatin-14 on both reversed-phase C1 8 and cation-exchange high-performance liquid chromatography columns. Milk, in contrast to plasma, contains only somatostatin-14-like material. Milk somatostatin was capable of inhibiting the basal and the prostaglandin-induced release of growth hormone from anterior pituitary cell cultures in a pattern similar to synthetic somatostatin-14. The concentrations of the peptide, as determined by radioimmunoassay, were found to be 11 3 pg/ml in human milk and 150 4.8 pg/ml (mean f range) in sheep milk. These values are severalfold higher than the corresponding concentration of the peptide in the plasma of these species. These findings are analogous to our previous observations concerning two other hypothalamic hormones, luliberin and thyroliberin [Baram, T., Koch, Y., Hazum, E. and Fridkin, M. (1977) Science (Wash. D C ) 198, 300-3021. The high concentration of somatostatin and other neuropeptides in milk implies either an active concentrating mechanism in the mammary gland or an additional extrahypothalamic source for the synthesis and release of these peptides.The extrahypothalamic distribution of somatostatin (SS), the growth-hormone-release-inhibiting factor, has been extensively reported [l -51. The finding that, in addition to the hypothalamus, a number of organs or tissues are involved in the synthesis of somatostatin, has been well established. The broad spectrum of biological effects exerted by this peptide [6] aroused much interest in the evaluation of its location and concentration in body tissues and fluids.Hormones are natural constituents of milk of various mammals [7]. Recently the presence of epidermal growth factor in human milk [8] and of opiate-like compounds in bovine milk [9] were reported. We and others have reported on immunoreactive and bioactive materials resembling luteinizing-hormone-releasing hormone (luliberin) and thyrotropin-releasing hormone (thyroliberin) in the milk of man, cow and rat [lo-131. It was found that the concentrations of these peptides in milk are significantly higher than the corresponding hormone levels in plasma [lo].We now report the presence of somatostatin in the milk of man and sheep. Comparative characterization of this peptide, along with synthetic, hypothalamic-like, somatostatin-14, has been carried out by chromatographic, radioimmunological and biological studies.Correspondence to Y . Koch MATERIALS AND METHODS Preparation of milk extractSheep milk was obtained from the Veterinary Institute, Beit Dagan, Israel, and human colostrum was obtained from the Department of Obstetrics and Gynecology, Wolfson Hospital, Bat-Yam, Israel. Human and sheep milk were defatted by centrifugation at 15000 rpm for 30 min at 4°C. Casein and other proteins were coagulated by acidification to pH 4 and removed by centrifugation. Defatted/de-casein...

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Physiological role of somatostatin in the control of growth hormone and thyrotropin secretion

Cited by 269 publications

References 18 publications

Effects of Somatostatin on the Growth Hormone‐Releasing Factor‐Induced Growth Hormone Secretion in Rats with Electrical and Chemical Inhibitions of Endogenous Growth Hormone‐Releasing Factor and Somatostatin

Effects of Somatostatin on the Growth Hormone‐Releasing Factor‐Induced Growth Hormone Secretion in Rats with Electrical and Chemical Inhibitions of Endogenous Growth Hormone‐Releasing Factor and Somatostatin

Acute Hyperglycemia and Activation of the .BETA.-Adrenergic System do not Exhibit Synergistic Inhibitory Actions on Thyrotropin-releasing Hormone (TRH)-induced Thyroid Stimulating Hormone (TSH) Secretion

Immunoreactive and biologically active somatostatin in human and sheep milk

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