Glucagon-Like Peptide-1 and Glucose-Dependent Insulin-Releasing Polypeptide Plasma Levels in Response to Nutrients

Herrmann, Christine; Göke, Rüdiger; Richter, G.; Fehmann, Hans-Christoph; Arnold, R.; Göke, Burkhard

doi:10.1159/000201231

Cited by 518 publications

(385 citation statements)

References 29 publications

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“…Three g/kg of glucose or water (~100µl) were injected over 30 seconds into the stomach catheter. For hormonal determinations, portal blood was collected after 15 minutes (considered as the time point giving the highest value of the time course (Herrmann et al, 1995)) onto a mixture of 1µg/ml of aprotinin and 0.1mM EDTA. The portal blood was sampled as previously described (Cani et al, 2006); 250µl of blood can be easily sampled using this technique.…”

Section: Glucose Tolerance Test (Gtt)mentioning

confidence: 99%

GLUT2 and the incretin receptors are involved in glucose-induced incretin secretion

Cani

Holst²,

Drucker

et al. 2007

Molecular and Cellular Endocrinology

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Glucagon-Like Peptide-1 (GLP-1) and Glucose-dependent Insulinotropic Polypeptide (GIP) are incretins secreted in response to oral glucose ingestion by intestinal L and K cells, respectively. The molecular mechanisms responsible for intestinal cell glucose sensing are unknown but could be related to those described for β-cells, brain and hepatoportal sensors.We determined the role of GLUT2, GLP-1 or GIP receptors in glucose-induced incretins secretion, in the corresponding knockout mice. GLP-1 secretion was reduced in all mutant mice, while GIP secretion did not require GLUT2. Intestinal GLP-1 content was reduced only in GIP and GLUT2 receptors knockout mice suggesting that this impairment could contribute to the phenotype. Intestinal GIP content was similar in all mice studied. Furthermore, the impaired incretins secretion was associated with a reduced glucose-stimulated insulin secretion and an impaired glucose tolerance in all mice. In conclusion, both incretin secretion depends on mechanisms involving their own receptors and GLP-1 further requires GLUT2.

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Section: Glucose Tolerance Test (Gtt)mentioning

confidence: 99%

GLUT2 and the incretin receptors are involved in glucose-induced incretin secretion

Cani

Holst²,

Drucker

et al. 2007

Molecular and Cellular Endocrinology

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“…Most studies have focused on responses to an oral glucose tolerance test, after which levels of GIP, GLP-1, and insulin rise, whereas glucagon levels are suppressed (4,18,20, 24). It is also known that fat and protein ingestion stimulate GLP-1 and GIP secretion (10,14,20,27). Less is known, however, regarding relationships between the incretin responses and changes in insulin and glucagon levels after meal or noncarbohydrate macronutrient ingestions.…”

mentioning

confidence: 99%

Incretin and islet hormonal responses to fat and protein ingestion in healthy men

Carr

Larsen²,

Winzell

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

166

129

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and glucose-dependent insulinotropic polypeptide (GIP) regulate islet function after carbohydrate ingestion. Whether incretin hormones are of importance for islet function after ingestion of noncarbohydrate macronutrients is not known. This study therefore examined integrated incretin and islet hormone responses to ingestion of pure fat (oleic acid; 0.88 g/kg) or protein (milk and egg protein; 2 g/kg) over 5 h in healthy men, aged 20 -25 yr (n ϭ 12); plain water ingestion served as control. Both intact (active) and total GLP-1 and GIP levels were determined as was plasma activity of dipeptidyl peptidase-4 (DPP-4). Following water ingestion, glucose, insulin, glucagon, GLP-1, and GIP levels and DPP-4 activity were stable during the 5-h study period. Both fat and protein ingestion increased insulin, glucagon, GIP, and GLP-1 levels without affecting glucose levels or DPP-4 activity. The GLP-1 responses were similar after protein and fat, whereas the early (30 min) GIP response was higher after protein than after fat ingestion (P Ͻ 0.001). This was associated with sevenfold higher insulin and glucagon responses compared with fat ingestion (both P Ͻ 0.001). After protein, the early GIP, but not GLP-1, responses correlated to insulin (r 2 ϭ 0.86; P ϭ 0.0001) but not glucagon responses. In contrast, after fat ingestion, GLP-1 and GIP did not correlate to islet hormones. We conclude that, whereas protein and fat release both incretin and islet hormones, the early GIP secretion after protein ingestion may be of primary importance to islet hormone secretion.insulin; glucagon; glucagon-like peptide-1; glucose-dependent insulinotropic polypeptide; incretins; man THE INTEGRATED ENDOCRINE RESPONSES TO FOOD INGESTION are dependent on both the size and the composition of a meal and include the postprandial release of the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) and the islet hormones insulin and glucagon (3,5,21,32). Most studies have focused on responses to an oral glucose tolerance test, after which levels of GIP, GLP-1, and insulin rise, whereas glucagon levels are suppressed (4,18,20, 24). It is also known that fat and protein ingestion stimulate GLP-1 and GIP secretion (10,14,20,27). Less is known, however, regarding relationships between the incretin responses and changes in insulin and glucagon levels after meal or noncarbohydrate macronutrient ingestions.GLP-1 and GIP are rapidly degraded by dipeptidyl peptidase-4 (DPP-4), which cleaves the two NH 2 -terminal amino acids of the peptides, making them largely inactive (9). Accurate estimation of the relationship between incretin hormone secretion and islet hormones therefore requires measurement of both the total and the active intact forms of the two incretins. How this is related to macronutrient ingestion is not known. Indeed, we recently showed in mice that protein ingestion increased intact incretin hormone levels compared with carbohydrate ingestion, and this was associated with reduced intestinal DPP-4...

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“…A study showed that high protein food intake increases the concentration of GLP-1 [79]. Cleavage of the preproglucagon resulted into two main bioactive forms of GLP-1, GLP-1 and the GLP-1 7-37 [80]. Both forms have a short biological half-life, because both of them are rapidly degraded during circulation by dipeptidil peptidase 4 (DPP4) [81].…”

Section: Glucagon-like Peptide-1mentioning

confidence: 99%

Role of gastrointestinal hormones in feeding behavior and obesity treatment

et al. 2015

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Food intake regulation is generally evaluated by many aspects consisting of complex mechanisms, including homeostatic regulatory mechanism, which is based on negative feedback, and hedonic regulatory mechanism, which is driven by a reward system. One important aspect of food intake regulation is the peripheral hormones that are secreted from the gastrointestinal tract. These hormones are secreted from enteroendocrine cells as feedback to nutrient and energy intake, and will communicate with the brain directly or via the vagus nerve. Gastrointestinal hormones are very crucial in maintaining a steady body weight, despite variations in nutrient intake and energy expenditure. In this review, we provide an overview of the regulation of feeding behavior by gut hormones, and its role in obesity treatments.

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Glucagon-Like Peptide-1 and Glucose-Dependent Insulin-Releasing Polypeptide Plasma Levels in Response to Nutrients

Cited by 518 publications

References 29 publications

GLUT2 and the incretin receptors are involved in glucose-induced incretin secretion

GLUT2 and the incretin receptors are involved in glucose-induced incretin secretion

Incretin and islet hormonal responses to fat and protein ingestion in healthy men

Role of gastrointestinal hormones in feeding behavior and obesity treatment

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