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Am J Physiol Gastrointest Liver Physiol 278: G946-G951, 2000;
0193-1857/00 $5.00
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Vol. 278, Issue 6, G946-G951, June 2000

Pramlintide, an amylin analog, selectively delays gastric emptying: potential role of vagal inhibition

Melvin Samsom1, Lawrence A. Szarka1, Michael Camilleri1, Adrian Vella2, Alan R. Zinsmeister3, and Robert A. Rizza2

1 Gastroenterology Research Unit, 2 Endocrine Research Unit, and 3 Section of Biostatistics, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905

The amylin analog pramlintide delays gastric emptying in type I diabetics. The effects of multiple doses of pramlintide and the mechanism of action in non-amylin-deficient humans are unknown. We investigated the effects of pramlintide on gastrointestinal and colonic transit and on the plasma pancreatic polypeptide response to the meal in a parallel-group dose-response study with subjects randomized to placebo, or 30 or 60 µg (tid, sc) of pramlintide. Pramlintide delayed gastric emptying [half-time (t1/2): 112 min (SE 8.7 min), 169 min (SE 12 min), or 177 min (SE 25 min) after placebo or 30- or 60-µg pramlintide treatment, respectively; P = 0.033]. Pramlintide did not significantly affect small bowel or colonic transit. Pancreatic polypeptide concentrations in the first postprandial hour were lower with pramlintide than with placebo (P < 0.01 for drug effect). An inverse correlation was observed between mean pancreatic polypeptide concentrations in the first postprandial hour and gastric emptying t1/2 [Spearman correlation coefficient (Rs) = 0.48; P = 0.044]. Pramlintide at 30 and 60 µg delays gastric emptying in healthy humans without affecting small bowel or colonic transit. Vagal inhibition is a potential mechanism of the effects of pramlintide on gastric emptying.

colonic transit; pancreatic polypeptide; glucose; diabetes mellitus


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