Effect of Somatostatin on Neurotensin-Induced Glucagon Release and Hyperglycemia

Ukai, Mitsuo; Inoue, Itaru; Itatsu, Takeharu

doi:10.1210/endo-100-5-1284

Cited by 36 publications

(11 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Neurotensin has been shown to induce hyperglycemia (3)(4)(5)(6)(7)(8) and this has been attributed to a stimulation of glucagon release associated with an inhibition of insulin release (3). It has recently been reported that neurotensin directly inhibits insulin release and stimulates glucagon release by isolated pancreatic islets (9).…”

mentioning

confidence: 99%

Effect of Neurotensin on Insulin, Glucagon, and Somatostatin Release from Isolated Pancreatic Islets*

et al. 1979

View full text Add to dashboard Cite

The effects of neurotensin on the release of insulin, glucagon, and somatostatin were investigated in isolated pancreatic islets prepared from 3- to 4-day-old rats and maintained in culture for 48 h before use. Islets were incubated for 20 and 60 min in the presence of 3 or 23 mM glucose with or without neurotensin. In 20-min incubations at 3 mM glucose, neurotensin (10-100 nM) increased the release of insulin, glucagon, and somatostatin by 60%, 90%, and 110%, respectively. These increases were not detected in 60-min incubations. Neurotensin (100 nM) inhibited the release of both insulin (by 60-90%) and somatostatin (by 100%) which was induced by 23 mM glucose in 60-min incubations; this inhibitory effect could be detected with neurotensin at a concentration of 1 nM. Neurotensin also significantly inhibited the elevations in glucagon, insulin, and somatostatin release induced by 20 mM arginine. It is concluded that neurotensin exerts a dual effect on the endocrine pancreas in vitro: 1) at low glucose concentration and over short term (20 min) incubations, the peptide stimulates insulin, glucagon, and somatostatin release; and 2) under stimulated conditions (high glucose or arginine), neurotensin inhibits insulin, glucagon, and somatostatin release.

show abstract

mentioning

confidence: 99%

Effect of Neurotensin on Insulin, Glucagon, and Somatostatin Release from Isolated Pancreatic Islets*

et al. 1979

View full text Add to dashboard Cite

show abstract

“…Neurotensin has been reported to stimulate release of thyrotropin in rats [49] and insulin and glucagon in dogs [50]. Other similar studies showed that neurotensin prevents atrophy of the intestinal mucosa associated with TPN and promotes the release of secretory IgA and IgM into the bile [51].…”

Section: Neurotensinmentioning

confidence: 99%

Factors Enhancing Intestinal Adaptation after Bowel Compensation

Botsios

Vasiliadis²

2003

Dig Dis

View full text Add to dashboard Cite

Intestinal failure (IF) refers to the condition in which certain causes lead to derangements in nutrient absorption capacity. Gut adaptation occurs in response to IF and it is both morphologic and physiologic in nature and can be mediated by growth factors and nutrients. Our paper reviews certain trophic growth factors that have important interactions relevant for intestinal growth, function and adaptation. Data Source: The literature was reviewed (data from both animal and human studies) and certain trophic factors that modulate intestinal adaptation are summarized. The factors reviewed are: epidermal growth factor, insulin-like growth factor I and II, transforming growth factor α and β, neurotensin, interleukin-11, glucagon-like peptide-2, keratinocyte growth factor, human growth hormone, short-chain fatty acids, and glutamine. Conclusions: Growth factors augment intestinal proliferation, diminish programmed apoptosis, and modulate the adaptive process. They also have the potential to improve nutrient absorption in some bowel disease. The enhancement of gut adaptation may allow patients to transition of parenteral/enteral to normal nutrition, in a shorter period of time, which reduce the rate of adverse effects caused by artificial nutrition and improve quality of life.

show abstract

“…On the other hand, Patton et al (1976) suggested that the hyperglycemic effect might be mediated by such a decrease in insulin, and/or an increase in glucagon. Hyperglucagonemia and hypoinsulinemia were observed in anesthetized rats , and moderate hyperinsulinemia and exaggerated hyperglucagonemia were also seen in dogs (Ukai et al 1977).…”

mentioning

confidence: 93%

“…In addition, neurotensin has been found to induce hyperglycemia in the rat and dog ; Nagai and Frohman 1976;Rosell et al 1976; Ukai et al 1977). This hyperglycemic effect seemed to be due to stimulation of hepatic glycogenolysis by its direct or indirect action.…”

mentioning

confidence: 99%

Hyperglycemic effect of neurotensin.

Yawata

Yamatani

Tominaga

et al. 1984

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

Mechanisms of hyperglycemic action of neurotensin were investigated in anesthetized dogs. The intravenous administration of neurotensin 1.0 ,u g/kg for 5 min induced an immediate decrease in arterial blood pressure and increases in levels of blood glucose, glucagon and insulin. Although blood levels of glucagon and insulin were greatly reduced and not elevated by neurotensin in the presence of somatostatin, the response of blood glucose to neurotensin was similar to that in the absence of somatostatin. The rise in blood glucose produced by intraportal injection of neurotensin was not greater than that produced by injection of the same dose of neurotensin into the femoral vein. The increments of glucagon and insulin secretion caused by the intraportal injection were also the same as those produced by the peripheral injection. Participation of antihypotensive mechanisms in the neurotensin-induced hyperglycemia was investigated by use of aadrenoceptor blockade and baroceptor denervation. Only the combination of somatostatin and a-adrenoceptor blockade or the denervation of baroceptors could suppress the hyperglycemic response to neurotensin. Stimulation of the secretion of anterior pituitary hormones by neurotensin infusion could not be recognized in the present experiments. These results suggested the following : 1) both glucagon and catecholamines may contribute to neurotensin-induced hyperglycemia, 2) neurotensin does not directly act on the liver, 3) catecholamine response could be mediated by baroceptor stimulation through hypotension, and 4) the hyperglycemic effect of anterior pituitary hormones does not participate in neurotensininduced hyperglycemia.

show abstract

Effect of Somatostatin on Neurotensin-Induced Glucagon Release and Hyperglycemia

Cited by 36 publications

References 0 publications

Effect of Neurotensin on Insulin, Glucagon, and Somatostatin Release from Isolated Pancreatic Islets*

Effect of Neurotensin on Insulin, Glucagon, and Somatostatin Release from Isolated Pancreatic Islets*

Factors Enhancing Intestinal Adaptation after Bowel Compensation

Hyperglycemic effect of neurotensin.

Contact Info

Product

Resources

About