Response of Circulating Somatostatin, Insulin, Gastrin and Gip, to Intraduodenal Infusion of Nutrients in Normal Man

Lucey, Michael R.; Fairclough, P. D.; Wass, John; Kwasowski, P.; Medbak, S.; Webb, Judith A. W.; Rees, Lesley

doi:10.1111/j.1365-2265.1984.tb03461.x

Cited by 34 publications

(10 citation statements)

References 20 publications

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“…These findings are in accord with in vivo data showing that fat is the most potent nutrient secretagogue of intestinal SLI (10,16,25). Of particular interest was the observation that oleic acid stimulated S28 secretion from D cells.…”

Section: Discussionsupporting

confidence: 79%

Nutrient and Peptide Regulation of Somatostatin-28 Secretion from Intestinal Cultures¹

Brubaker

Gronau²,

Sylvia

et al. 1998

Endocrinology

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Of the two known forms of intestinal somatostatin, somatostatin-28 (S28) and S14, S28 predominates in the distal mucosa, whereas S14 is localized in the foregut. Although S14 release has been well studied, little is known about the factors regulating secretion of S28 from the intestine. Therefore, fetal rat intestinal cultures, which have been previously demonstrated to synthesize and secrete predominantly S28, were treated with potential nutrient, neuromodulator/ transmitter, and peptide secretagogues (n ϭ 4 -6/experiment). Oleic acid dose dependently stimulated the release of somatostatin-like immunoreactivity (SLI) to 272 Ϯ 81% of the control value at 1.5 ϫ 10 Ϫ4 M (P Ͻ 0.01). Gel permeation analysis (n ϭ 3) demonstrated that this increment was accounted for not only by an increase in the release of S28, but also by an increase in that of S14, such that the secretion of both peptides was increased in parallel. Of the neuromodulators tested, only the enteric peptide gastrin-releasing peptide stimulated intestinal SLI secretion, to 386 Ϯ 60% of the control value at 10 Ϫ6 M (P Ͻ 0.001); similar to oleic acid, the effects on S28 and S14 were equivalent. Galanin, vasoactive intestinal peptide, bethanechol, and epinephrine did not affect SLI release. The duodenal hormone secretin also stimulated SLI release to 310 Ϯ 78% of the control value at 10 Ϫ6 M (P Ͻ 0.001); however, secretin caused a preferential release of S14 over that of S28 (S14, 7.8 Ϯ 2.8-fold; S28, 1.5 Ϯ 0.1-fold). In contrast, gastrin, cholecystokinin, glucose-dependent insulinotropic peptide, neurotensin, peptide YY, epidermal growth factor, and transforming growth factor-␣ had no effect on intestinal SLI release. Thus, luminal nutrients and neuro/endocrine peptides exert differential effects on S28 release from the rat intestine compared with those on S14. These findings implicate S28 as a distinct regulatory peptide in the physiological setting. (Endocrinology 139: 148 -155, 1998) A LTHOUGH widely distributed in the brain, pancreas, and peripheral autonomic nervous system, the gastrointestinal tract provides the largest source of somatostatin in the periphery (1-3). Within the gastrointestinal tract, differential posttranslational processing of prosomatostatin generates two major biologically active peptides, somatostatin-14 (S14) and S28, the distribution of which forms a gradient along the aboral axis. In the mucosa of the stomach and duodenum, S14 is the major product of processing, whereas S28 predominates in the D cells of the distal jejunum and ileum (1-4). S14 is also distributed throughout the length of the small intestine within the myenteric plexi. Both peptides have potent inhibitory effects on digestive functions, including gastric and pancreatic exocrine secretion, neuro/endocrine peptide release, and intestinal growth (5). Of particular note are studies suggesting that S28, rather than S14, may be the physiological regulator of postprandial insulin secretion in humans (6, 7). Although regulation of S14 secretion from the st...

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Section: Discussionsupporting

confidence: 79%

Nutrient and Peptide Regulation of Somatostatin-28 Secretion from Intestinal Cultures¹

Brubaker

Gronau²,

Sylvia

et al. 1998

Endocrinology

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“…Hence, our finding that plasma NT-proSST is elevated in patients with vascular dementia but not Alzheimer's disease adds not only valuable information in order to distinguish between dementia subtypes but also might offer a potential diagnostic tool to predict dementia development. It has previously been reported that plasma somatostatin levels are significantly elevated by ingestion of food containing much fat [24]. In addition, circadian rhythm and older age have been described as confounders for plasma somatostatin level [25,26].…”

Section: Discussionmentioning

confidence: 99%

N-Terminal Prosomatostatin and Risk of Vascular Dementia

et al. 2017

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Background: Increased somatostatin plasma concentration has been found in patients with vascular dementia. However, it is unknown whether or not somatostatin levels may predict dementia development in the general population. To this end, we sought to assess the association of circulating N-terminal prosomatostatin (NT-proSST) with incident dementia among community-dwelling older adults. Methods: In the prospective population-based Malmö Preventive Project, 5,347 study participants (mean age: 69 ± 6years; 70% men) provided plasma for the determination of NT-proSST concentration. Of these, 373 participants (7%) were diagnosed with dementia (120 Alzheimer's disease, 83 vascular, 102 mixed, and 68 other aetiology) during a follow-up period of 4.6 ± 1.3 years. The association of NT-proSST with the risk of dementia and its subtypes was studied using multivariable-adjusted Cox regression models controlling for age, gender, body mass index, systolic blood pressure, antihypertensive treatment, smoking, diabetes, lipid levels and prevalent stroke. Results: Higher levels of NT-proSST were significantly associated with an increased risk of vascular dementia (hazard ratio [HR] per 1 SD: 1.29; 95% CI 1.05-1.59; p = 0.016), whereas no association was observed with Alzheimer's disease (HR per 1 SD: 0.99; 95% CI 0.81-1.20; p = 0.91), all-cause dementia (HR per 1 SD: 1.04; 95% CI 0.94-1.16; p = 0.44), and mixed dementia (HR per 1 SD: 0.98; 95% CI 0.79-1.21; p = 0.84). Levels of NT-proSST above 563 pmol/L (highest quartile) conferred distinctly increased risk of vascular dementia (HR 1.66; 95% CI 1.05-2.63; p = 0.029) compared with lower values. Conclusions: Higher levels of circulating N-terminal-prosomatostatin are associated with increased incidence of vascular dementia. Our findings might be of importance for the understanding of dementia development in older adults.

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“…Several studies have documented a rise in somatostatinlike immunoreactivity after nutrient intake (10)(11)(12)(13), and fat has been shown to be the most potent nutrient stimulus to somatostatin-like immunoreactivity release (12,13). We have recently reported that, in healthy men, ingestion of a mixed meal results in a two-to threefold rise in S-28, without changes in S-14 (14).…”

Section: Introductionmentioning

confidence: 99%

A physiologic role for somatostatin 28 as a regulator of insulin secretion.

D’Alessio¹,

Sieber²,

Beglinger³

et al. 1989

J. Clin. Invest.

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Somatostatin 28 (S-28) is a peptide produced in the intestinal tract which rises in the circulation during nutrient absorption. We tested the hypothesis that S-28 regulates B-cell function by (a) studying the effects on insulin secretion of "physiologic" infusions of S-28 and (b) measuring insulin responses during elevated nutrient-stimulated endogenous S-28 levels. (a) Synthetic S-28 was infused on separate days into six healthy men at rates of 25 and 50 ng/kg per h which mimicked postprandial levels. Subjects were given a bolus of glucose (0.1 g/kg) after 120 min. Insulin responses during S-28 infusions were compared to a control study using a saline infusion in the same individuals. Glucose-stimulated insulin secretion was inhibited during the infusion of 50 ng/kg per h S-28 when compared to control (P < 0.05). (b) Insulin secretion during elevations of endogenous S-28 was studied in healthy men who received a bolus of 2.5 g arginine (n = 14) or 25 U of secretin (n = 8) 120 min after swallowing 50 g fat, or, on a separate day, an equivalent volume of water. S-28 levels rose significantly after fat ingestion but did not change after water. Arginine and secretin-stimulated insulin secretion was inhibited following ingestion of fat compared with intake of water (P < 0.05). Arginineenhanced glucagon secretion was not changed by fat ingestion. We conclude that elevations in plasma S-28 levels, occurring during the postprandial state, attenuate B-cell secretion and this peptide may be a physiologic modulator of nutrient-stimulated insulin release.

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Response of Circulating Somatostatin, Insulin, Gastrin and Gip, to Intraduodenal Infusion of Nutrients in Normal Man

Cited by 34 publications

References 20 publications

Nutrient and Peptide Regulation of Somatostatin-28 Secretion from Intestinal Cultures¹

Nutrient and Peptide Regulation of Somatostatin-28 Secretion from Intestinal Cultures¹

N-Terminal Prosomatostatin and Risk of Vascular Dementia

A physiologic role for somatostatin 28 as a regulator of insulin secretion.

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Response of Circulating Somatostatin, Insulin, Gastrin and Gip, to Intraduodenal Infusion of Nutrients in Normal Man

Cited by 34 publications

References 20 publications

Nutrient and Peptide Regulation of Somatostatin-28 Secretion from Intestinal Cultures1

Nutrient and Peptide Regulation of Somatostatin-28 Secretion from Intestinal Cultures1

N-Terminal Prosomatostatin and Risk of Vascular Dementia

A physiologic role for somatostatin 28 as a regulator of insulin secretion.

Contact Info

Product

Resources

About

Nutrient and Peptide Regulation of Somatostatin-28 Secretion from Intestinal Cultures¹

Nutrient and Peptide Regulation of Somatostatin-28 Secretion from Intestinal Cultures¹