Mannitol and glucose: effects on gastric acid secretion and endogenous gastric inhibitory polypeptide (GIP).
Serum gastric inhibitory polypeptide was measured in dogs prepared with Heidenhain pouches and Mann-Bollman fistulae following the intraduodenal (ID) infusion of isotonic saline, 20% glucose, or 20% mannitol. Following ID 20% glucose, serum GIP concentrations rose significantly (P less than 0.05) between 30 and 120 min and there was a significant inhibition (P less than 0.05) of acid secretion in the Heidenhain pouches between 15 and 75 min. A good correlation (r = 0.925) was found between the rise in serum GIP and the inhibition of acid secretion. Although neither ID isotonic saline nor 20% mannitol stimulated GIP release, the latter produced a significant (P less than 0.05) inhibition of acid secretion between 60 and 105 min. We conclude: (1) the inhibitory effect of acid secretion following ID glucose is mediated in part by the release of endogenous GIP; (2) glucose and mannitol probably inhibit gastric acid secretion by different mechanisms.
D000818:Animals; D004285:Dogs; D004386:Duodenum; D005749:Gastric Inhibitory Polypeptide / Q000097:blood* / Q000502:physiology; D005750:Gastric Juice / Q000378:metabolism*; D005753:Gastric Mucosa / Q000378:metabolism*; D005768:Gastrointestinal Hormones / Q000097:blood*; D005947:Glucose / Q000494:pharmacology*; D005950:Glucose Solution, Hypertonic / Q000008:administration & dosage / Q000494:pharmacology*; D007441:Intubation, Gastrointestinal; D008353:Mannitol / Q000008:administration & dosage / Q000494:pharmacology*; D010418:Pentagastrin / Q000494:pharmacology; D012636:Secretory Rate / Q000187:drug effects; D012965:Sodium Chloride / Q000494:pharmacology
D005768:Gastrointestinal Hormones; D005950:Glucose Solution, Hypertonic; D008353:Mannitol; D012965:Sodium Chloride; D005749:Gastric Inhibitory Polypeptide; D010418:Pentagastrin; D005947:Glucose