Electron immunohistochemical evidence for the human intestinal I cell as the source of CCK.

Buchan, Alison; Polak, Julia M.; Solcia, Enrico; Capella, Carlo; Hudson, Debra V.; Pearse, A. G. E.

doi:10.1136/gut.19.5.403

Cited by 112 publications

(53 citation statements)

References 10 publications

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“…This augmentation of insulin secretion is due to the secretion and action of gut hormones with insulinotropic activity, namely gastric inhibitory polypeptide (GIP,' also called glucose-dependent insulinotropic hormone; 5, 6) from the upper gut (7) and glucagon-like peptide 1 [7-36 amide] (GLP-1 [7-36 amide]; proglucagon 78-107 amide; 8-11) from the lower gut (12,13). In type-2 diabetic patients, the incretin effect is reduced or lost (4,14).…”

Section: Introductionmentioning

confidence: 99%

Preserved incretin activity of glucagon-like peptide 1 [7-36 amide] but not of synthetic human gastric inhibitory polypeptide in patients with type-2 diabetes mellitus.

Nauck

Heimesaat²,

Ørskov³

et al. 1993

J. Clin. Invest.

1,520

1,158

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In type-2 diabetes, the overall incretin effect is reduced. 17-36 amidel dose-dependently augmented insulin secretion (insulin, C-peptide) in both groups (P < 0.05). With GIP, the maximum effect in type-2 diabetic patients was significantly lower (by 54%; P < 0.05) than in normal subjects. With GLP-1 17-36 amidel type-2 diabetic patients reached 71% of the increments in C-peptide of normal subjects (difference not significant). Glucagon was lowered during hyperglycemic clamps in normal subjects, but not in type-2 diabetic patients, and further by GLP-1 17-36 amidel in both groups (P < 0.05), but not by GIP. In conclusion, in mild type-2 diabetes, GLP-1 17-36 amidel, in contrast to GIP, retains much of its insulinotropic activity. It also lowers glucagon concentrations. (J. Clin. Invest. 1993. 91:301-307.) Key words: enteroinsular axis* gastric inhibitory peptide -glucagon-like peptide 1 17-36 amidel * hyperglycemic clamp * incretin hormones -pancreatic glucagon

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Section: Introductionmentioning

confidence: 99%

Preserved incretin activity of glucagon-like peptide 1 [7-36 amide] but not of synthetic human gastric inhibitory polypeptide in patients with type-2 diabetes mellitus.

Nauck

Heimesaat²,

Ørskov³

et al. 1993

J. Clin. Invest.

1,520

1,158

View full text Add to dashboard Cite

show abstract

“…CCK is the anorexigenic peptide that has been more thoroughly studied 14 ; this hormone is released by I-cells into the duodenum in response to intra-luminal lipids and proteins. 15,16 The CCK inhibitory effects on food intake are thought to be mediated via CCK1 receptors on vagal afferents.…”

Section: Introductionmentioning

confidence: 99%

The Bitter Taste Receptor Agonist Quinine Reduces Calorie Intake and Increases the Postprandial Release of Cholecystokinin in Healthy Subjects

Andreozzi

Sarnelli

Pesce

et al. 2015

J Neurogastroenterol Motil

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Background/AimsBitter taste receptors are expressed throughout the digestive tract. Data on animals have suggested these receptors are involved in the gut hormone release, but no data are available in humans. Our aim is to assess whether bitter agonists influence food intake and gut hormone release in healthy subjects. MethodsTwenty healthy volunteers were enrolled in a double-blind cross-over study. On 2 different days, each subject randomly received an acid-resistant capsule containing either placebo or 18 mg of hydrochloride (HCl) quinine. After 60 minutes, all subjects were allowed to eat an ad libitum meal until satiated. Plasma samples were obtained during the experiment in order to evaluate cholecystokinin (CCK) and ghrelin levels. Each subject was screened to determine phenylthiocarbamide (PTC) tasting status. ResultsCalorie intake was significantly lower when subjects received HCl quinine than placebo (514 ± 248 vs 596 ± 286 kcal; P = 0.007). Significantly higher CCK ΔT90 vs T0 and ΔT90 vs T60 were found when subjects received HCl quinine than placebo (0.70 ± 0.69 vs 0.10 ± 0.86 ng/mL, P = 0.026; 0.92 ± 0.75 vs 0.50 ± 0.55 ng/mL, P = 0.033, respectively). PTC tasters ingested a significantly lower amount of calories when they received HCl quinine compared to placebo (526 ± 275 vs 659 ± 320 kcal; P = 0.005), whereas no significant differences were found for PTC non-tasters (499 ± 227 vs 519 ± 231 kcal; P = 0.525).Paolo Andreozzi, et al Journal of Neurogastroenterology and Motility 512 ConclusionsThis study showed that intra-duodenal release of a bitter compound is able to significantly affect calorie intake and CCK release after a standardized meal. Our results suggest that bitter taste receptor signaling may have a crucial role in the control of food intake. (J Neurogastroenterol Motil 2015;21:511-519)

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“…Glucose-dependent insulinotropic polypeptide (GIP) is a 42 amino acid incretin hormone synthesised by enteroendocrine K-cells (Buchan et al 1978), which upon secretion modulates pancreatic -cell insulin release (Creutzfeldt 2001). GIP exerts its potentiating effects on glucoseinduced insulin release via interaction with specific -cell GIP receptors (Usdin et al 1993).…”

Section: Introductionmentioning

confidence: 99%

Improved biological activity of Gly2- and Ser2-substituted analogues of glucose-dependent insulinotrophic polypeptide

Gault

Flatt²,

Harriott

et al. 2003

Journal of Endocrinology

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Electron immunohistochemical evidence for the human intestinal I cell as the source of CCK.

Cited by 112 publications

References 10 publications

Preserved incretin activity of glucagon-like peptide 1 [7-36 amide] but not of synthetic human gastric inhibitory polypeptide in patients with type-2 diabetes mellitus.

Preserved incretin activity of glucagon-like peptide 1 [7-36 amide] but not of synthetic human gastric inhibitory polypeptide in patients with type-2 diabetes mellitus.

The Bitter Taste Receptor Agonist Quinine Reduces Calorie Intake and Increases the Postprandial Release of Cholecystokinin in Healthy Subjects

Improved biological activity of Gly2- and Ser2-substituted analogues of glucose-dependent insulinotrophic polypeptide

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