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Published online June 20, 2008
Diabetes 57:2332-2340, 2008
DOI: 10.2337/db07-0758
© 2008 by the American Diabetes Association
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Cholinergic Regulation of Ghrelin and Peptide YY Release May Be Impaired in Obesity

Christina Maier1, Michaela Riedl1, Greisa Vila1, Peter Nowotny1, Michael Wolzt2, Martin Clodi1, Bernhard Ludvik1, and Anton Luger1

1 Clinical Division of Endocrinology and Metabolism, Department of Medicine III, Medical University of Vienna, Vienna, Austria
2 Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria

Corresponding author: Christina Maier, christina.maier{at}meduniwien.ac.at

OBJECTIVE—Ghrelin and peptide YY (PYY) are both hormones derived from the gastrointestinal tract involved in appetite regulation. The cholinergic part of the vagal nerve is involved in the regulation of glucose and insulin. The aim of this study was to examine the effects of the cholinergic antagonist atropine on ghrelin, PYY, glucose, and insulin under basal conditions and after meal ingestion in lean and obese subjects.

REASEARCH DESIGN AND METHODS—Eight lean and eight obese subjects were included in a randomized, double-blind, placebo-controlled crossover study with 4 study days in randomized order (atropine/placebo ± breakfast). Plasma ghrelin, PYY, insulin, and glucose were measured. Hunger and satiety feelings were rated on a 10-cm visual analog scale.

RESULTS—In lean individuals, atropine led to a decrease in ghrelin concentrations comparable and nonadditive with breakfast ingestion and a significant decrease in both basal and meal-induced PYY concentrations. In obese subjects, atropine did not significantly change ghrelin or PYY concentrations, whereas it induced a comparable increase in heart rate and meal-induced glucose concentrations in the two study groups. Only lean, not obese, subjects experienced sustained feelings of satiety after breakfast.

CONCLUSIONS—The impaired cholinergic regulation of the postprandial drop in ghrelin concentrations and rise in PYY concentrations might be part of the deregulated food intake in obese subjects.


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Copyright © 2008 by the American Diabetes Association.