Gastrointestinal somatostatin: Distribution, secretion and physiological significance

McIntosh, Christopher H.S.

doi:10.1016/0024-3205(85)90576-4

Cited by 75 publications

(43 citation statements)

References 158 publications

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“…Up to 70% of ghrelin production is derived from the stomach (Date et al 2000), although the entire amount of circulating ghrelin can be accounted for by the splanchnic bed (Moller et al 2003). Various gastric secretory and hormonal functions are sensitive to the chemical properties of food within the stomach (McIntosh 1985, Hakanson et al 1986). However, gastric ghrelin-producing cells situated at the base of the mucosal layer are primarily of the closed type, and as such, are not in direct contact with the gastric lumen (Date et al 2000, Rindi et al 2002, Sakata et al 2002.…”

Section: Discussionmentioning

confidence: 99%

Vagal stimulation exaggerates the inhibitory ghrelin response to oral fat in humans

Heath¹,

Jones²,

Frayn³

et al. 2004

Journal of Endocrinology

118

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Ghrelin, the growth hormone secretagogue receptor ligand, is a key regulator of adiposity and food intake. However, the regulation of ghrelin in response to dietary fat intake remains largely unclear. Furthermore, cephalic elevation of ghrelin may influence fat absorption and postprandial lipaemia. Therefore, the aim of this study was to examine the effect of fat ingestion and vagal stimulation on the regulation of plasma ghrelin.Vagal stimulation was achieved by modified sham feeding (MSF). Eight healthy subjects (four male/four female) consumed a 50 g fat load on two separate occasions. On one occasion, the fat load was preceded by the MSF of a meal for 1 h. Blood, appetite and breath were analysed for 5 h postprandially.A 25% (S.E.M. 3·4) suppression in ghrelin concentration was observed after fat ingestion (P,0·001), without an increase in glucose or insulin. MSF in addition to oral fat enhanced ghrelin suppression further, as well as elevating plasma triacylglycerol (P,0·001) and reducing appetite (P,0·001). The fasting ghrelin concentration was inversely correlated with gastric half-emptying time (P=0·036).We conclude that ghrelin release may be influenced directly by both vagal stimulation and oral fat ingestion.

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Section: Discussionmentioning

confidence: 99%

Vagal stimulation exaggerates the inhibitory ghrelin response to oral fat in humans

Heath¹,

Jones²,

Frayn³

et al. 2004

Journal of Endocrinology

118

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“…In addition, somatostatin is produced by enteric nerve endings innervating the intestine (11)(12)(13)(14). These diverse cellular somatostatin sources may actually control the amount, location, and timing of somatostatin secretion.…”

Section: Discussionmentioning

confidence: 99%

“…A candidate neuropeptide that may be involved in such neuronal regulation is somatostatin, a 14-aa cyclic peptide that is released from nerve endings that reach the intestine and thus may affect various cells within the mucosa. Within the intestine, somatostatin is also secreted from nonneuronal cells distributed throughout the length of the gastrointestinal tract, specifically in the antrum and duodenum, as well as in the small intestine and colon (11)(12)(13)(14). The idea that various cells within the intestine can respond to somatostatin is supported by studies showing that various cell types found throughout the intestine, including epithelial cells, expressed somatostatin receptors (15)(16)(17).…”

mentioning

confidence: 99%

Somatostatin Through Its Specific Receptor Inhibits Spontaneous and TNF-α- and Bacteria-Induced IL-8 and IL-1β Secretion from Intestinal Epithelial Cells

Chowers

Cahalon

Lahav

et al. 2000

The Journal of Immunology

111

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Intestinal epithelial cells secrete proinflammatory cytokines and chemokines that are crucial in mucosal defense. However, this secretion must be tightly regulated, because uncontrolled secretion of proinflammatory mediators may lead to chronic inflammation and mucosal damage. The aim of this study was to determine whether somatostatin, secreted within the intestinal mucosa, regulates secretion of cytokines from intestinal epithelial cells. The spontaneous as well as TNF-α- and Salmonella-induced secretion of IL-8 and IL-1β derived from intestinal cell lines Caco-2 and HT-29 was measured after treatment with somatostatin or its synthetic analogue, octreotide. Somatostatin, at physiological nanomolar concentrations, markedly inhibited the spontaneous and TNF-α-induced secretion of IL-8 and IL-1β. This inhibition was dose dependent, reaching >90% blockage at 3 nM. Furthermore, somatostatin completely abrogated the increased secretion of IL-8 and IL-1β after invasion by Salmonella. Octreotide, which mainly stimulates somatostatin receptor subtypes 2 and 5, affected the secretion of IL-8 and IL-1β similarly, and the somatostatin antagonist cyclo-somatostatin completely blocked the somatostatin- and octreotide-induced inhibitory effects. This inhibition was correlated to a reduction of the mRNA concentrations of IL-8 and IL-1β. No effect was noted regarding cell viability. These results indicate that somatostatin, by directly interacting with its specific receptors that are expressed on intestinal epithelial cells, down-regulates proinflammatory mediator secretion by a mechanism involving the regulation of transcription. These findings suggest that somatostatin plays an active role in regulating the mucosal inflammatory response of intestinal epithelial cells after physiological and pathophysiological stimulations such as bacterial invasion.

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“…Moreover, concentrations of insulin were reduced from 30 to 60 min in LPS-treated steers, which indicates that another factor is involved in regulating release of insulin. One candidate factor is somatostatin (SS), which is synthesized in neurons in the hypothalamus (Leshin et al 1994) and in D-cells of the pancreas and gastrointestinal tract (McIntosh 1985, Schusdziarra 1996. In rats, injections of LPS stimulate release of SS, which is probably released from the pancreas (Yelich et al 1993, Yelich & Witek-Janusek 1994.…”

Section: Figurementioning

confidence: 99%

Estradiol/progesterone implants increase food intake, reduce hyperglycemia and increase insulin resistance in endotoxic steers

McMahon

Elsasser²,

Gunter³

et al. 1998

Journal of Endocrinology

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High doses of lipopolysaccharide (LPS) induce transient hyperglycemia, then chronic hypoglycemia and increased insulin resistance. In addition, appetite is reduced, while body temperature and concentrations of cortisol and tumor necrosis factor alpha (TNF ) are elevated. Furthermore, concentrations of GH and IGF-I are reduced in cattle. The objectives of this study were to determine whether a gonadal steroid implant (20 mg estrogen and 200 mg progesterone) given to endotoxemic steers would: (1) reduce hyperglycemia, reduce hypoglycemia, reduce insulin resistance, (2) reduce changes in concentrations of GH and IGF-I, (3) reduce inappetence and reduce concentrations of blood urea nitrogen (BUN) and nonesterified fatty acids (NEFA), and (4) reduce fever and concentrations of TNF and cortisol. Holstein steers were assigned within a 2 2 factorial arrangement of treatments as follows (n=5 per group): C/C, no steroid and vehicle; S/C, steroid and vehicle; C/E, no steroid and LPS (1 µg/kg body weight (BW), i.v.); S/E, steroid and endotoxin. Steroid implants were given at 20 weeks of age (day 0) and serial blood samples (15 min) were collected on day 14 for 8 h, with vehicle or LPS injected after 2 h. Intravenous glucose tolerance tests (100 mg/kg BW) were carried out at 6 h and 24 h. Hyperglycemia was 67% lower (P<0·05) in S/E-compared with C/E-treated steers between 30 and 150 min after i.v. injection of LPS.Hypoglycemia developed after 4 h and insulin resistance was greater in S/E-compared with C/E-treated steers (P<0·05) at 6 and 24 h. Concentrations of IGF-I were restored earlier in steroid-treated steers than in controls. Concentrations of GH were not affected by steroids, but increased 1 h after injection of LPS, then were reduced for 2 h. Appetite was greater (P<0·05) in S/E-(2·1% BW) compared with C/E-treated steers (1·1% BW) (pooled ...=0·3). Concentrations of NEFA increased after injecting LPS, but concentrations were lower (P<0·05) in S/E-compared with C/E-treated steers. LPS did not affect concentrations of BUN, but concentrations were lower in steroid-treated steers. Steroids did not affect body temperature or concentrations of TNF and cortisol. In summary, gonadal steroids reduce hyperglycemia, reduce inappetence and tissue wasting, but increase insulin resistance. Furthermore, concentrations of IGF-I are restored earlier in steroid-treated than in non-steroid-treated steers injected with LPS. It is concluded that gonadal steroids reduce severity of some endocrine and metabolic parameters associated with endotoxemia. However, it is unlikely that gonadal steroids acted via anti-inflammatory and immunosuppressive actions of glucocorticoids or through reducing concentrations of cytokines.

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Gastrointestinal somatostatin: Distribution, secretion and physiological significance

Cited by 75 publications

References 158 publications

Vagal stimulation exaggerates the inhibitory ghrelin response to oral fat in humans

Vagal stimulation exaggerates the inhibitory ghrelin response to oral fat in humans

Somatostatin Through Its Specific Receptor Inhibits Spontaneous and TNF-α- and Bacteria-Induced IL-8 and IL-1β Secretion from Intestinal Epithelial Cells

Estradiol/progesterone implants increase food intake, reduce hyperglycemia and increase insulin resistance in endotoxic steers

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