Mechanisms of peptide YY release induced by an intraduodenal meal in rats: neural regulation by proximal gut |
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Authors: | Fu-Cheng Xiaomei Anini Younes Chariot Jacques Castex Nathalie Galmiche Jean-Paul Rozé C |
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Institution: | (1) Clinique des Maladies de l’Appareil Digestif, CHU H?tel Dieu, F-44035 Nantes, France, FR;(2) Pharmacologie, INRA, F-31300 Toulouse, France, FR;(3) INSERM U410, Faculté de Médecine X Bichat, BP 416, F-75870 Paris Cedex 18, France, FR |
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Abstract: | Peptide YY (PYY) release in anaesthetized rats was studied during the 2 h following the intraduodenal administration of a
semi-liquid meal of 21 kJ. Surgical and pharmacological manipulations were performed in order to analyse the mechanisms of
PYY release. Postprandial PYY release was suppressed or strongly decreased by caecocolonectomy, truncal vagotomy, tetrodotoxin,
hexamethonium, sensory denervation by perivagal capsaicin, and by the NO-synthase inhibitor L-N-arginine methyl ester, while atropine, adrenergic blockers, antagonists of type-A or type-B cholecystokinin (CCK) receptors
or bombesin receptors had no effect. Comparing the digestive transit of the semi-liquid meal with the amount of PYY contained
in the small bowel wall showed that nutrients had not reached the area rich in cells containing PYY by 30 min, the time at
which there was a large PYY release in plasma. By 120 min, the meal front had travelled 72% of the small intestine length,
just beginning to reach the PYY-rich part of the ileum. We conclude that the main postprandial PYY release studied in this
model comes from ileal and colonic L-cells indirectly stimulated through a neural mechanism originating in the proximal gut
and involving sensory vagal fibres, nicotinic synapses and NO release, while CCK and bombesin do not seem to be physiologically
involved.
Received: 17 July 1996 / Received after revision: 11 October 1996 / Accepted: 18 October 1996 |
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Keywords: | Hormone release Duodenum Sensory nerves Nitric oxide Antagonists and inhibitors |
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