Gastrointestinal satiety signals in humans — Physiologic roles for GLP-1 and PYY ?

  title={Gastrointestinal satiety signals in humans — Physiologic roles for GLP-1 and PYY ?},
  author={Christoph Beglinger and Lukas P. Degen},
  journal={Physiology \& Behavior},

Intestinal GLP-1 and satiation: from man to rodents and back

The available evidence for intestinal GLP-1 is reviewed to fulfill a number of established empirical criteria for assessing whether a hormone inhibits eating by eliciting physiological satiation in man and rodents.

Gut induced biomarkers of appetite and satiety

The findings indicate that the receptor is not alone responsible for peptide secretion; it is rather a complex interaction between different receptor mechanisms.

Gastrointestinal targets to modulate satiety and food intake

The role of enteroendocrine cells in the gastrointestinal tract as chemoreceptors that sense intraluminal contents and induce changes in food intake through the release of signalling substances, such as satiety hormones is discussed.

Effect of glucagon-like peptide-1 receptor antagonism on appetite and food intake in healthy men.

The effect of ex9-39 on PYY secretion supports an autoinhibitory feedback mechanism that controls L cell secretion; the effect on insulin and glucagon confirms the role of GLP-1 in glycemic control through its action on pancreatic α and β cells.

Ghrelin, CCK, GLP-1, and PYY(3-36): Secretory Controls and Physiological Roles in Eating and Glycemia in Health, Obesity, and After RYGB.

Gastric emptying, the detection of specific digestive products by small intestinal enteroendocrine cells, and synergistic interactions among different GI loci all contribute to the secretion of ghrelin, CCK, GLP-1, and PYY(3-36).

Neuroendocrine control of satiation

This review is not comprehensive; rather, it discusses only what it considers the best-understood mechanisms of satiation, with a special focus on normally operating physiological mechanisms.

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.

Glucagon-like peptide-1, a gastrointestinal hormone with a pharmaceutical potential.

    J. Holst
    Medicine, Biology
    Current medicinal chemistry
  • 1999
It is currently being investigated how GLP-1 or analogues thereof can be employed in practical diabetes therapy, and promising solutions include the development of stable analogues and inhibitors of the degrading enzyme.

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.

Effects of fat digestion on appetite, APD motility, and gut hormones in response to duodenal fat infusion in humans.

In conclusion, lipase inhibition attenuates the effects of duodenal fat on antropyloroduodanal motility, appetite, and CCK and glucagon-like peptide-1 secretion.

Gut peptides and postprandial satiety.

There are three reports thatCCK decreases the size of a test meal in lean and obese humans, which suggests that CCK or the other peptides may be useful in treating human obesity and bulimia.

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

The results show that GLP-1 enhanced satiety and reduced energy intake and thus may play a physiological regulatory role in controlling appetite and energy intake in humans.

Effects of glucagon-like peptide-1(7–36)amide on motility and sensation of the proximal stomach in humans

GLP-1 is a candidate physiological inhibitory regulator of fundus motility that allows the stomach to afford a larger volume without increase in sensation.

Endogenous glucagon-like peptide 1 controls endocrine pancreatic secretion and antro-pyloro-duodenal motility in humans

GLP-1 is suggested as a true incretin hormone and enterogastrone in humans because it tonically inhibits antroduodenal motility and mediates the postprandial inhibition of antral and stimulation of pyloric motility.

Inhibition of food intake in obese subjects by peptide YY3-36.

It is found that obese subjects were not resistant to the anorectic effects of PYY, and endogenous PYY levels were low in obese subjects, suggesting that PYY deficiency may contribute to the pathogenesis of obesity.

Cholecystokinin: a putative satiety signal.

It is believed that CCK should be considered a putative satiety signal and an interesting therapeutic alternative to administration of exogenous CCK is the release of endogenous CCK by nutrients such as amino acids which can be ingested as preloads which release significant amounts of CCK.