Glucagon-like peptide 1 promotes satiety and suppresses energy intake in humans.

  title={Glucagon-like peptide 1 promotes satiety and suppresses energy intake in humans.},
  author={Anne Flint and Anne Raben and Arne Astrup and Jj. Holst},
  journal={The Journal of clinical investigation},
  volume={101 3},
We examined the effect of intravenously infused glucagon-like peptide 1 (GLP-1) on subjective appetite sensations after an energy-fixed breakfast, and on spontaneous energy intake at an ad libitum lunch. 20 young, healthy, normal-weight men participated in a placebo-controlled, randomized, blinded, crossover study. Infusion (GLP-1, 50 pmol/ kg.h or saline) was started simultaneously with initiation of the test meals. Visual analogue scales were used to assess appetite sensations throughout the… 

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Glucagon-like peptide-1 promotes satiety and reduces food intake in patients with diabetes mellitus type 2.

A marked effect of GLP-1 on appetite is demonstrated by showing enhanced satiety and reduced energy intake in patients with diabetes type 2.

Energy intake and appetite are suppressed by glucagon-like peptide-1 (GLP-1) in obese men.

It is demonstrated that GLP-1 decreases feelings of hunger and reduces energy intake in obese humans and one possible mechanism for this finding might be an increased satiety primarily mediated by gastric vagal afferent signals.

The effect of physiological levels of glucagon-like peptide-1 on appetite, gastric emptying, energy and substrate metabolism in obesity

It is concluded that GLP-1 in physiological concentrations powerfully reduces the rate of entry of nutrients into the circulation by a reduction of gastric emptying rate in obese subjects and may be beneficial in weight reduction.

No effect of glucagon-like peptide-1 on short-term satiety and energy intake in man

Doubts are cast on whether GLP-1 is a major satiety factor in man, although a raised circulating plasma glucose level, as would normally occur postprandially, might be necessary for GLp-1 to increase satiety.

No effect of physiological concentrations of glucagon-like peptide-2 on appetite and energy intake in normal weight subjects†

Circulating GLP-2 in physiological concentrations does not seem to play a significant role in human appetite regulation.

rapid communication Glucagon-like peptide-1 promotes satiety and reduces food intake in patients with diabetes mellitus type 2

A marked effect of GLP-1 on appetite is demonstrated by showing enhanced satiety and reduced energy intake in patients with diabetes type 2.

Glucagon-like peptide-1: a potent regulator of food intake in humans

Intravenous infusions of GLP-1 decrease spontaneous food intake even at physiological plasma concentrations, implying an important role for GLp-1 in the regulation of the early satiety response in humans.

The effect of glucagon-like peptide-1 on energy expenditure and substrate metabolism in humans

Peripheral GLp-1 decreased DIT and carbohydrate oxidation, probably secondary to a delayed absorption of nutrients, since substrate and hormone concentrations in plasma were suppressed during GLP-1 infusion.

Do the actions of glucagon-like peptide-1 on gastric emptying, appetite, and food intake involve release of amylin in humans?

GLP-1 exerts its effect on gastric emptying, appetite, food intake, and glucagon secretion directly, although secretion of amylin may contribute to some of these effects in healthy control subjects.



Glucagon-like peptide 1 inhibition of gastric emptying outweighs its insulinotropic effects in healthy humans.

It is suggested that despite the known insulinotropic actions of GLP-1-(7-36) amide and -(7-37), the net effect of administering GLp-1 with a meal is no change or a reduction in meal-related insulin responses.

Attenuated GLP-1 secretion in obesity: cause or consequence?

Postprandial GLP-1 secretion in response to oral carbohydrate is considerably attenuated in obese subjects and it is suggested that both this fall and the overall reduction in GLp-1 values in obese Subjects may be related to an increase in plasma non-esterified fatty acids.

Effect of glucagon-like peptide-1 (proglucagon 78-107amide) on hepatic glucose production in healthy man.

Central administration of GLP-1-(7-36) amide inhibits food and water intake in rats.

In conclusion, GLP-1 may play a physiological role in regulation of both ingestion and the water and salt homeostasis and had no effect in behavioral assays measuring exploratory locomotor activity and conditioned taste aversion.

Secretion of the incretin hormones glucagon-like peptide-1 and gastric inhibitory polypeptide correlates with insulin secretion in normal man throughout the day.

The notion that GLP-1 and GIP are important incretin hormones is supported, as their plasma concentrations increased significantly and in parallel with insulin in response to all three meals.

Reduction of the Incretin Effect in Rats by the Glucagon-Like Peptide 1 Receptor Antagonist Exendin (9–39) Amide

The data support the concept that GLP-1 is an important incretin factor and exendin (9–39) amide is a useful GLp-1 antagonist for in vivo studies.

Glucose intolerance but normal satiety in mice with a null mutation in the glucagon–like peptide 1 receptor gene

It is demonstrated that GLP1 plays a central role in the regulation of glycemia; however, disruption of GLP 1/GLP1R signaling in the central nervous system is not associated with perturbation of feeding behavior or obesity in vivo.

A role for glucagon-like peptide-1 in the central regulation of feeding

It is reported here that intracerebroventricular (ICV) GLP-1 powerfully inhibits feeding in fasted rats, and this findings suggest that central GLp-1 is a new physiological mediator of satiety.

Glucagon-like peptide-1 is a physiological incretin in rat.

Glucagon-like peptide-1 7-36 amide (GLP-1) has been postulated to be the primary hormonal mediator of the entero-insular axis but evidence has been indirect. The discovery of exendin (9-39), a GLP-1

Glucagon-like peptide-1 7-36 amide and peptide YY have additive inhibitory effect on gastric acid secretion in man.

The results indicate that GLP-1 and PYY have an important role in the physiologic control of gastric acid secretion and suggest that the interaction betweenglucagon-like peptide-1 7-36 amide in man is of the additive type.