The vagus is inhibitory of the late postprandial insulin secretion in conscious pigs

Blat, Sophie; Guérin, Sylvie; Chauvin, Alain; Sève, Bernard; Cuber, Jean‐Claude; Malbert, Charles‐Henri

doi:10.1016/s1566-0702(02)00184-4

Cited by 8 publications

(7 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Based on studies in rodents, it has been claimed that the vagus nerve plays an important role in GLP-1 secretion (58). However, vagotomy and vagus stimulation in pigs did not affect secretion of either GLP-1 or the other incretin hormone, glucose-dependent insulinotropic polypeptide (GIP) (6). Furthermore, in another detailed study in pigs, there were no changes in GLP-1 or GLP-2 and only weak effects on GIP secretion after electrical stimulation of the vagal trunks at the level of the diaphragm (28) despite clear effects on the release of vagal neurotransmitters.…”

Section: Discussionmentioning

confidence: 99%

The effect of exogenous GLP-1 on food intake is lost in male truncally vagotomized subjects with pyloroplasty

Plamboeck

Veedfald

Deacon

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

151

104

View full text Add to dashboard Cite

Rapid degradation of glucagon-like peptide-1 (GLP-1) by dipeptidyl peptidase-4 suggests that endogenous GLP-1 may act locally before being degraded. Signaling via the vagus nerve was investigated in 20 truncally vagotomized subjects with pyloroplasty and 10 matched healthy controls. Subjects received GLP-1 (7-36 amide) or saline infusions during and after a standardized liquid mixed meal and a subsequent ad libitum meal. Despite no effect on appetite sensations, GLP-1 significantly reduced ad libitum food intake in the control group but had no effect in the vagotomized group. Gastric emptying was accelerated in vagotomized subjects and was decreased by GLP-1 in controls but not in vagotomized subjects. Postprandial glucose levels were reduced by the same percentage by GLP-1 in both groups. Peak postprandial GLP-1 levels were approximately fivefold higher in the vagotomized subjects. Insulin secretion was unaffected by exogenous GLP-1 in vagotomized subjects but was suppressed in controls. GLP-1 significantly reduced glucagon secretion in both groups, but levels were approximately twofold higher and were nonsuppressible in the early phase of the meal in vagotomized subjects. Our results demonstrate that vagotomy with pyloroplasty impairs the effects of exogenous GLP-1 on food intake, gastric emptying, and insulin and glucagon secretion, suggesting that intact vagal innervation may be important for GLP-1's actions.

show abstract

Section: Discussionmentioning

confidence: 99%

The effect of exogenous GLP-1 on food intake is lost in male truncally vagotomized subjects with pyloroplasty

Plamboeck

Veedfald

Deacon

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

151

104

View full text Add to dashboard Cite

show abstract

“…All this suggests that acetylcholine could be a transmitter in a neural stimulatory pathway for GLP-1 secretion. However, another study in conscious pigs indicated that the vagus nerve is not involved in control of GLP-1 release (18). Finally, in recent extensive studies employing both isolated perfused porcine ileum and intact pigs, a variety of neurally active agents as well as electrical stimulation of the abdominal vagal trunks were employed to investigate the importance of the neural regulation (100).…”

Section: Regulation Of Secretionmentioning

confidence: 99%

The Physiology of Glucagon-like Peptide 1

Holst¹

2007

Physiological Reviews

2,709

2,385

View full text Add to dashboard Cite

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.

show abstract

“…All this suggests that ACh could be a transmitter in a neural stimulatory pathway for GLP-1 secretion. However, a more recent study in conscious pigs (6) indicated that the vagus nerve is not involved in control of GLP-1 release.…”

mentioning

confidence: 97%

“…However, the response to a meal is usually rapid, with increases in the plasma concentration occurring within a few minutes after the start of meal ingestion (6,10,24,34,38), before the bulk of the meal is thought to have reached the lower gut. This suggests that a neural and/or an endocrine pathway from the upper part of the gastrointestinal tract to the lower gut may exist.…”

mentioning

confidence: 99%

Neural regulation of glucagon-like peptide-1 secretion in pigs

Hansen

Lampert

Mineo

et al. 2004

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

like peptide (GLP)-1 is secreted rapidly from the intestine postprandially. We therefore investigated its possible neural regulation. With the use of isolated perfused porcine ileum, GLP-1 secretion was measured in response to electrical stimulation of the mixed, perivascular nerve supply and infusions of neuroactive agents alone and in combination with different blocking agents. Electrical nerve stimulation inhibited GLP-1 secretion, an effect abolished by phentolamine. Norepinephrine inhibited secretion, and phentolamine abolished this effect. GLP-1 secretion was stimulated by isoproterenol (abolished by propranolol). Acetylcholine stimulated GLP-1 secretion, and atropine blocked this effect. Dimethylphenylpiperazine stimulated GLP-1 secretion. In chloralose-anesthetized pigs, however, electrical stimulation of the vagal trunks at the level of the diaphragm had no effect on GLP-1 or GLP-2 and weak effects on glucose-dependent insulinotropic peptide and somatostatin secretion, although this elicited a marked atropine-resistant release of the neuropeptide vasoactive intestinal polypeptide to the portal circulation. Thus GLP-1 secretion is inhibited by the sympathetic nerves to the gut and may be stimulated by intrinsic cholinergic nerves, whereas the extrinsic vagal supply has no effect. somatostatin; nerve stimulation; enteric nervous system; vasoactive intestinal polypeptide; incretin hormones GLUCAGON-LIKE PEPTIDE (GLP)-1 is a peptide primarily produced in the lower part of the gut (reviewed in Ref. 22). It is known as an incretin hormone (stimulating insulin secretion) (27) and thought to be part of the "ileal brake" mechanism (inhibition of upper gut motility and secretion elicited by the presences of unabsorbed nutrients in the ileum) (28,32,44). Thus infusions of GLP-1 have been shown to reduce appetite and energy intake in humans (14). Relatively little is known about the mechanisms that regulate GLP-1 secretion in pigs and humans.The presence of unabsorbed nutrients in the lumen seems to be an important stimulus for GLP-1 secretion in rats (38), pigs (23), and humans (28). However, the response to a meal is usually rapid, with increases in the plasma concentration occurring within a few minutes after the start of meal ingestion (6,10,24,34,38), before the bulk of the meal is thought to have reached the lower gut. This suggests that a neural and/or an endocrine pathway from the upper part of the gastrointestinal tract to the lower gut may exist.In rats, glucose-dependent insulinotropic peptide (GIP) has been shown to stimulate GLP-1 secretion (9,20,35,38), although recent studies have indicated that a neural pathway involving the vagus nerve (2, 39) might predominate compared with a direct endocrine pathway. Infusions of muscarinic cholinergic agonists into isolated perfused rat ileum and colon resulted in stimulation of GLP-1 secretion (9,19,35), and studies in anesthetized rats and in fetal rat intestinal cells suggested that both M1 and M2 muscarinic receptors could be involved in control of GLP-1 rel...

show abstract

The vagus is inhibitory of the late postprandial insulin secretion in conscious pigs

Cited by 8 publications

References 39 publications

The effect of exogenous GLP-1 on food intake is lost in male truncally vagotomized subjects with pyloroplasty

The effect of exogenous GLP-1 on food intake is lost in male truncally vagotomized subjects with pyloroplasty

The Physiology of Glucagon-like Peptide 1

Neural regulation of glucagon-like peptide-1 secretion in pigs

Contact Info

Product

Resources

About