Ileal carbohydrates inhibit cholinergically stimulated exocrine pancreatic secretion in humans

Gröger, G.; Unger, Abraham; Holst, Jens J.; Goebell, H.; Layer, Peter

doi:10.1007/bf02803901

Cited by 32 publications

(18 citation statements)

References 37 publications

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“…It was first noted that GLP-1 inhibits gastrin-induced acid secretion in humans (261), and subsequently demonstrated that GLP-1 also inhibits meal-induced secretion as well as gastric emptying and pancreatic secretion (327). The effect on pancreatic exocrine secretion was first suspected to be secondary to the inhibition of gastric emptying, but in subsequent studies, GLP-1 was demonstrated to also inhibit pancreatic secretion in response to intraduodenal stimulation (84). The inhibitory effect of GLP-1 on acid secretion could be elicited by physiological elevations of the GLP-1 concentrations in plasma and was, remarkably, additive to the inhibitory effects of PYY, which is released from the L-cell in parallel with GLP-1 (324).…”

Section: E Effects On the Gastrointestinal Tractmentioning

confidence: 99%

The Physiology of Glucagon-like Peptide 1

Holst¹

2007

Physiological Reviews

2,703

2,385

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Glucagon-like peptide 1 (GLP-1) is a 30-amino acid peptide hormone produced in the intestinal epithelial endocrine L-cells by differential processing of proglucagon, the gene which is expressed in these cells. The current knowledge regarding regulation of proglucagon gene expression in the gut and in the brain and mechanisms responsible for the posttranslational processing are reviewed. GLP-1 is released in response to meal intake, and the stimuli and molecular mechanisms involved are discussed. GLP-1 is extremely rapidly metabolized and inactivated by the enzyme dipeptidyl peptidase IV even before the hormone has left the gut, raising the possibility that the actions of GLP-1 are transmitted via sensory neurons in the intestine and the liver expressing the GLP-1 receptor. Because of this, it is important to distinguish between measurements of the intact hormone (responsible for endocrine actions) or the sum of the intact hormone and its metabolites, reflecting the total L-cell secretion and therefore also the possible neural actions. The main actions of GLP-1 are to stimulate insulin secretion (i.e., to act as an incretin hormone) and to inhibit glucagon secretion, thereby contributing to limit postprandial glucose excursions. It also inhibits gastrointestinal motility and secretion and thus acts as an enterogastrone and part of the “ileal brake” mechanism. GLP-1 also appears to be a physiological regulator of appetite and food intake. Because of these actions, GLP-1 or GLP-1 receptor agonists are currently being evaluated for the therapy of type 2 diabetes. Decreased secretion of GLP-1 may contribute to the development of obesity, and exaggerated secretion may be responsible for postprandial reactive hypoglycemia.

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Section: E Effects On the Gastrointestinal Tractmentioning

confidence: 99%

The Physiology of Glucagon-like Peptide 1

Holst¹

2007

Physiological Reviews

2,703

2,385

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“…PYY is secreted predominantly from endocrine cells in the ileum and colon and PP from endocrine cells in the pancreas, both in response to all three macronutrients, fat, carbohydrate, and protein, with fat being the most potent stimulus and carbohydrate the least potent or, possibly, impotent (2,16,29,33). Enteral administration of free fatty acids, including dodecanoate (3) or oleate (22), are known to be potent stimuli of PYY secretion.…”

mentioning

confidence: 99%

Fat digestion is required for suppression of ghrelin and stimulation of peptide YY and pancreatic polypeptide secretion by intraduodenal lipid

Feinle‐Bisset

Patterson²,

Ghatei³

et al. 2005

American Journal of Physiology-Endocrinology and Metabolism

141

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-Stimulation of cholecystokinin and glucagon-like peptide-1 secretion by fat is mediated by the products of fat digestion. Ghrelin, peptide YY (PYY), and pancreatic polypeptide (PP) appear to play an important role in appetite regulation, and their release is modulated by food ingestion, including fat. It is unknown whether fat digestion is a prerequisite for their suppression (ghrelin) or release (PYY, PP). Moreover, it is not known whether small intestinal exposure to fat is sufficient to suppress ghrelin secretion. Our study aimed to resolve these issues. Sixteen healthy young males received, on two separate occasions, 120-min intraduodenal infusions of a long-chain triglyceride emulsion (2.8 kcal/min) 1) without (condition FAT) or 2) with (FAT-THL) 120 mg of tetrahydrolipstatin (THL, lipase inhibitor), followed by a standard buffet-style meal. Blood samples for ghrelin, PYY, and PP were taken throughout. FAT infusion was associated with a marked, and progressive, suppression of plasma ghrelin from t ϭ 60 min (P Ͻ 0.001) and stimulation of PYY from t ϭ 30 min (P Ͻ 0.01). FAT infusion also stimulated plasma PP (P Յ 0.01), and the release was immediate. FAT-THL completely abolished the FAT-induced changes in ghrelin, PYY, and PP. In response to the meal, plasma ghrelin was further suppressed, and PYY and PP stimulated, during both FAT and FAT-THL infusions. In conclusion, in healthy humans, 1) the presence of fat in the small intestine suppresses ghrelin secretion, and 2) fat-induced suppression of ghrelin and stimulation of PYY and PP is dependent on fat digestion. lipase inhibition; gut hormone secretion A NUMBER OF GASTROINTESTINAL PEPTIDES play a role in the regulation of energy intake in humans, including cholecystokinin (CCK) (19, 27), glucagon-like peptide-1 (GLP-1) (13, 17), peptide YY (PYY) (4), pancreatic polypeptide (PP) (5), and ghrelin (42). The secretion of CCK, GLP-1, and PYY from intestinal cells, and PP from the pancreas, is stimulated by meal ingestion or infusion of nutrients into the small intestine (10,18,21,29). In contrast, ghrelin is secreted by the stomach, and plasma concentrations increase during fasting and are suppressed by a meal (7,8).Plasma ghrelin concentrations decrease rapidly following food ingestion, and there is evidence that ghrelin plays a role in meal initiation (7,8). Intravenously administered ghrelin has been shown to stimulate appetite and increase food intake in humans (42). Both carbohydrate and fat, when ingested orally, suppress ghrelin secretion (9, 15), whereas protein may stimulate ghrelin secretion (9) or have no effect (15). Although until recently it has been unclear whether the suppressive effect of carbohydrate and fat on ghrelin secretion is mediated by the presence of nutrients in the stomach, the small intestine, and/or the circulation, recent animal (41) and human (30) studies indicate that the interaction of nutrients with the small intestine is important in the glucose-induced modulation of ghrelin secretion. In rats, the prevention of gastric empty...

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“…Previous experiment suggested a similar response to carbohydrates as administration of isotonic solutions of starch and maltose significantly inhibited pancreatic enzyme output stimulated with an intravenous infusion of the cholinergic agonist carbachol (Groger et al 1997) or by duodenal perfusion with a mixture of essential amino acids (450 μmol/min) (Layer et al 1990). Inhibitory effects of various enteral diets on the exocrine pancreatic secretion were demonstrated also in other reports using feeding tubes placed 10 cm or more distal to the ligament of Treitz (Pfeiffer et al 1993;Vidon et al 1988;Vu et al 1999).…”

Section: Applications To Other Conditionsmentioning

confidence: 95%

Enteral and Parenteral Nutrition in Postoperative Pancreatic Fistula

Kłęk¹

2015

Diet and Nutrition in Critical Care

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Ileal carbohydrates inhibit cholinergically stimulated exocrine pancreatic secretion in humans

Cited by 32 publications

References 37 publications

The Physiology of Glucagon-like Peptide 1

The Physiology of Glucagon-like Peptide 1

Fat digestion is required for suppression of ghrelin and stimulation of peptide YY and pancreatic polypeptide secretion by intraduodenal lipid

Enteral and Parenteral Nutrition in Postoperative Pancreatic Fistula

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