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A Meta-Analysis of the Effect of Glucagon-Like Peptide-1 (7–36) Amide on Ad Libitum Energy Intake in Humans

Research Department of Human Nutrition, Centre for Food Research (C.V., A.F., A.A.), The Royal Veterinary and Agricultural University, DK-1958 Frederiksberg C, Denmark; Division of Surgery, Karolinska Institute (E.N.), Danderyd Hospital, SE-182 88 Daderyd, Sweden; School of Biological Science (S.J.L., L.M.M.), University of Surrey, Guildford GU2 5XH, United Kingdom; Division of Gastroenterolgy (J.-P.G., C.B.), University Hospital, CH-4031 Basel, Switzerland; Department of Gastroenterology and Hepatology (P.M.H.), Karolinska Hospital, SE-171 76 Stockholm, Sweden; and Department of Medical Physiology, The Panum Institute (J.J.H.), University of Copenhagen, DK-2200 Copenhagen N, Denmark

Address all correspondence and requests for reprints to: Prof. Arne Astrup, Research Department of Human Nutrition, The Royal Veterinary and Agricultural University, Rolighedsvej 30, DK-1958 Frederiksberg C, Denmark. E-mail: ast{at}kvl.dk

Abstract

Seven studies have now been published pertaining to the acute effect of iv administration of glucagon-like peptide-1 (7–36) amide on ad libitum energy intake. In four of these studies energy intake was significantly reduced following the glucagon-like peptide-1 infusion compared with saline. In the remaining studies, no significant effect of glucagon-like peptide-1 could be shown. Lack of statistical power or low glucagon-like peptide-1 infusion rate may explain these conflicting results.

Our aim was to examine the effect of glucagon-like peptide-1 on subsequent energy intake using a data set composed of subject data from previous studies and from two as yet unpublished studies. Secondly, we investigated whether the effect on energy intake is dose dependent and differs between lean and overweight subjects.

Raw subject data on body mass index and ad libitum energy intake were collected into a common data set (n = 115), together with study characteristics such as infusion rate, duration of infusion, etc. From four studies with comparable protocol the following subject data were included if available: plasma concentrations of glucagon-like peptide-1, subjective appetite measures, well-being, and gastric emptying rate of a meal served at the start of the glucagon-like peptide-1 infusion.

Energy intake was reduced by 727 kJ (95% confidence interval, 548–908 kJ) or 11.7% during glucagon-like peptide-1 infusion. Although the absolute reduction in energy intake was higher in lean (863 kJ) (634–1091 kJ) compared with overweight subjects (487 kJ) (209–764 kJ) (P = 0.05), the relative reduction did not differ between the two groups (13.2% and 9.3%, respectively). Stepwise regression analysis showed that the glucagon-like peptide-1 infusion rate was the only independent predictor of the reduction in energy intake during glucagon-like peptide-1 (7–36) amide infusion (r = 0.4, P < 0.001). Differences in mean plasma glucagon-like peptide-1 concentration on the glucagon-like peptide-1 and placebo day (n = 43) were related to differences in feelings of prospective consumption (r = 0.40, P < 0.01), fullness (r = 0.38, P < 0.05), and hunger (r = 0.26, P = 0.09), but not to differences in ad libitum energy intake. Gastric emptying rate was significantly lower during glucagon-like peptide-1 infusion compared with saline. Finally, well-being was not influenced by the glucagon-like peptide-1 infusion.

Glucagon-like peptide-1 infusion reduces energy intake dose dependently in both lean and overweight subjects. A reduced gastric emptying rate may contribute to the increased satiety induced by glucagon-like peptide-1.

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