ECE2010 Poster Presentations Obesity (50 abstracts)
Glucagon stimulates cholecystokinin secretion in humans
Ayman Arafat 1 , Bärbel Otto 2 , Aikaterini Adamidou 1 , Joachim Spranger 1 , Martin Weickert 1, , Matthias Möhlig 1 & Andreas Pfeiffer 1
1Department of Endocrinology, Diabetes and Nutrition, Charité-University Medicine Berlin, Campus Benjamin Franklin, Berlin, Germany; 2Medical Department-Innenstadt, University Hospital Munich, Munich, Germany; 3Warwickshire Institute for the Study of Diabetes, Endocrinology and Metabolism, University Hospitals Coventry and Warwickshire, Coventry, UK.
Objectives: Gastrointestinal hormones are known to modulate satiety. The mechanisms underlying the impact of glucagon on satiety are so far unknown. However, it can be postulated that the glucagon-induced reduction in hunger feeling is mediated through changes in Cholecystokinin (CCK), which is known to play a role in meal termination. It was the aim of the present study to evaluate the impact of glucagon on CCK and the modulation of these effects in obesity.
Methods: In a cross-over design we studied the endocrine and metabolic responses to intramuscular glucagon or placebo administration in 12 obese subjects (6 males; BMI 33.9±1.6 kg/m2) and in 14 lean controls (6 males; 21.6±0.5 kg/m2). CCK was measured using highly-sensitive radioimmunoassay.
Results: Age, fasting glucose and glucagon levels were comparable in both groups. Obese subjects showed higher insulin and CCK levels as compared to lean controls (P<0.05). After glucagon administration, insulin and glucagon levels increased in both study groups (P<0.001), and these changes were comparable between obese and lean subjects. Glucagon significantly increased CCK in both obese (CCK–AUC240: 421.3±87.7 (glucagon) versus 201.5±22.7 (placebo), P<0.05) and in lean controls (553.2±73.1 versus 190.4±17.4, P<0.001).
Conclusions: We show that glucagon significantly increased CCK in both obese and lean subjects. However, further studies are needed to evaluate the mechanisms underlying this effect and to address the pathophysiological role of glucagon-induced changes in CCK with respect to satiety.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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