Somatostatin — both hormone and neurotransmitter?

Luft, Rolf; Efendić, Suad; Hökfelt, Tomas

doi:10.1007/bf00429702

Cited by 117 publications

(39 citation statements)

References 97 publications

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“…The relatively close relationship between the peripheral plasma somatostatin levels achieved in the high dose group and the reported portal plasma levels in other conditions such as diabetes (11,23), which are associated by reduced hepatic T4-5'-deiodinase activity, suggests that the demonstrated somatostatin effect could be physiological. The plasma levels achieved in the low dose group were similar to those required to induce other reported effects of somatostatin (11,25,26).…”

Section: Discussionsupporting

confidence: 77%

“…Somatostatin is known to influence nutriment absorption and carbohydrate metabolism (10,25,26). However, the demonstrated absence of weight loss and the normal hepatic glycogen content in the somatostatin-treated glucose-fed and -refed animals in the present study suggest that there was no impairment of glucose absorption.…”

Section: Discussioncontrasting

confidence: 61%

“…Thus, somatostatin did most likely impair the metabolism of glucose. Hyperglycemia consequent to somatostatin treatment is thought to reflect increased hepatic glucose output and decreased peripheral uptake of glucose (25). However, these actions of somatostatin have been attributed to its modulation of the endocrine system (insulin and glucagon) rather than to a direct effect on glucose metabolism (33).…”

Section: Discussionmentioning

confidence: 99%

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Somatostatin inhibits rat hepatic T4-5'-deiodinase. The effect is independent of the associated hypoinsulinemia.

Gavin¹,

Moeller²

1983

J. Clin. Invest.

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A B S T R A C T Somatostatin decreases the serum 3,5,3'-triiodothyronine (T3) concentration in athyreotic subjects treated with L-thyroxine (T4). The present study was performed to determine the effect of somatostatin on T4-5'-deiodinase activity in rat tissue homogenate preparations. This enzyme is an important regulator of T3 production. Continuous somatostatin infusion at high dose (4 ag/kg per min subcutaneously) and low dose (0.8 ,ug/kg per min subcutaneously) for 48-72 h significantly increased (P < 0.001) the mean aorta plasma somatostatin-like immunoreactivity concentration to 786±65 and 448±58 pg/mi, respectively compared with the normal mean of 69±17 pg/ml in the carbohydrate-fed rat (20% glucose in water ad lib.). The mean hepatic T4-5'-deiodinase activity at both 48 h (100±5 pmol/min per 100 mg protein) and 72 h (90±7 pmol/min per 100 mg protein) was significantly reduced in the high-dose group (P < 0.005), compared with the mean enzyme activity in the glucose-fed control group (138±6 pmol/min per 100 mg protein). There was a negative correlation (r = -0.9, P < 0.01) between the alterations in the peripheral plasma somatostatinlike immunoreactivity concentration and hepatic T4-5'-deiodinase activity. High-dose somatostatin did not consistently lower the serum T3 concentration in the glucose-fed rat. Somatostatin had no effect on pituitary T4-5'-deiodinase activity in the glucose-fed rat. Highdose somatostatin also significantly inhibited (P < 0.01) the glucose-refeeding reactivation of hepatic T4-5'-deiodinase in the 72-h-fasted rat. The mean enzyme activity after 96 h was 96±8 pmol/min per 100 mg protein compared with 127±4 pmol/min per 100 mg protein in the refed control group. Somatostatin had a similar inhibitory effect on serum T3. There was a positive correlation (r = 0.5, P < 0.01) between the somatostatin-induced alterations in serum T3 and hepatic T4-5'-deiodinase during refeeding. A significant positive correlation (r = 07, P < 0.005) was noted between the somatostatin effect on hepatic T4-5'-deiodinase activity and the induced hypoinsulinemia in the fed group. In addition, a significant negative correlation (r = -0.9, P < 0.001) was noted between the suppressed enzyme activity and the serum glucose/insulin ratio in the refed group. However, although low-dose somatostatin also induced the same degree of hypoinsulinemia (P < 0.05) in the fed and refed groups it had no effect on hepatic T4-5'-deiodinase activity. Furthermore, despite the induction of hyperinsulinemia during refeeding, the highdose somatostatin inhibitory effect on enzyme activity persisted.Thus, somatostatin inhibited hepatic T4-5'-deiodinase activity in the carbohydrate-fed rat and prevented the carbohydrate-refeeding normalization of enzyme activity in the 72-h-fasted rat. The effect of somatostatin on enzyme activity was independent of the associated hypoinsulinemia. In the carbohydrate-fed animal the somatostatin effect was selective, as the hormone had no effect on pituitary T4-5'-deiodinase activity. These data suggest ...

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Section: Discussionsupporting

confidence: 77%

Section: Discussioncontrasting

confidence: 61%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Somatostatin inhibits rat hepatic T4-5'-deiodinase. The effect is independent of the associated hypoinsulinemia.

Gavin¹,

Moeller²

1983

J. Clin. Invest.

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“…16 It may regulate the rate of nutrient entry from the intestine 17 and the demonstration that physiologic concentrations of SLI may suppress insulin and glucagon secretion is consistent with a possible hormonal role for the peptide. 18 In the present study, we have demonstrated that the circulating concentrations of SLI 28 and SLI 14 are similar.…”

Section: Resultsmentioning

confidence: 76%

Evidence for the presence of somatostatin 28 in plasma

Shoelson¹,

Polonsky²,

Docherty³

et al. 1982

Diabetes

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SUMMARYSomatostatin-like immunoreactivity (SLI) from dog and rat plasma eluted from Biogel P-6 columns as three distinct peaks. A large-molecular-weight peak was present in the void volume of the column, an intermediate-sized peak (SLI 28) coeluted with synthetic somatostatin 28 (S-28), and a small-molecular-weight peak (SLI 14 ) coeluted with SRIF. Material from the SLI 28 peak diluted in parallel to the S-28 standard in the radioimmunoassay and behaved identically to S-28 on high pressure liquid chromatography (HPLC). Levels of SLI 28 in the portal vein were consistently greater than the simultaneously measured peripheral levels (portal peripheral ratio 2.2 ± 0.2). Venous samples drawn from multiple sites suggested that SLI 28 is secreted by the duodenum and/or pancreas and the intestine. This data is consistent with the possibility that S-28 is a hormone distinct from SRIF. DIABETES 37: 474-477, May 1982.

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“…The islet cells thus represent one of the important members of paraneurons (FUJITA, 1976(FUJITA, , 1977. Secretion of somatostatin, a neurohormone, in the islet D cells (LUFT et al, 1978) and Glutaraldehyde and osmium possible occurrence of insulin and glucagon in certain neurons (TAGER et al, 1976;HAVRANKOVA et al, 1978) seem to symbolize the paraneuronal nature of islet cells. The long known structure called the neuro-insular complex (SIMARD, 1935;FUJITA, 1959) which is formed by a mixture and direct juxtaposition of neurons, Schwann cells and islet cells has called attention anew as an evidence of the paraneuronal nature of islet cells (FUJITA, 1976;.…”

Section: Islet Cells As Paraneuronsmentioning

confidence: 99%

Proposal of a Neurosecretory System in the Pancreas

Fujita

Kobayashi

1979

Arch. Histol. Jap., Arch. Histol. Jpn

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Summary. The nerve fibers supplying the islets of the dog pancreas were examined by electron microscopy. Axons with swollen portions containing various types of synaptic vesicles, including a cholinergic type, two varieties of presumable aminergic type and a possible peptidergic type, rush to the pericapillary space to end there, whereas only a small part of them seem to terminate on the endocrine cells of the islet.Schwann cell cytoplasm invests the axons and often separates these from the endocrine cells. The terminal portions filled with vesicles usually become free of the Schwann sheath on the side facing the blood capillary. Here the neuronal secretions are believed to be released into the blood stream through the pored endothelium of the capillary.The neurosecretions, together with the islet hormones are distributed to the exocrine pancreas in high concentrations via the insulo-acinar portal system. It seems thus sufficient for the nerves to supply the islet in order to control the exocrine function of the pancreas.During the three decades since the establishment of the hypothalamo-hypophyseal neurosecretory system by BARGMANN (1949), the concept and criteria of neurosecretion have changed a great deal (LEDERIS, 1974;SANO, 1978). BARGMANN and SCHARRER (1951) regarded that stain-technologically demonstrable secretory granules are essential for a neurosecretory cell, but later this criterion had to be abandoned as newly discovered neurosecretory system producing and transporting releasing hormones from the hypothalamus to the hypophyseal portal vessels revealed no stainable granules. Recent advance in the knowledge of peptidergic neurons and of aminecontaining neurons occurring in different central and peripheral nervous tissues caused further confusion to the concept of neurosecretion. In agreement with SANO (1978), the last reliable criterion of neurosecretion (in higher vertebrates) must be that the neuronal secretions are released into the circulation and this is morphologically reflected in that the nerve terminals are not related to their target organ or cell but end in the perivascular (especially pericapillary) space.In the course of our electron microscope study of the dog pancreas, we recently noticed that numerous nerve terminals occur in the pericapillary spaces of the islet. Also by re-examining the electron micrographs which we produced for our previous *This paper is dedicated to the memory of the late Professor Wolfgang BARGMANN. 277

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Somatostatin — both hormone and neurotransmitter?

Cited by 117 publications

References 97 publications

Somatostatin inhibits rat hepatic T4-5'-deiodinase. The effect is independent of the associated hypoinsulinemia.

Somatostatin inhibits rat hepatic T4-5'-deiodinase. The effect is independent of the associated hypoinsulinemia.

Evidence for the presence of somatostatin 28 in plasma

Proposal of a Neurosecretory System in the Pancreas

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