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Endocrine Abstracts (2012) 29 S29.3

Faculty of Science, University of Copenhagen, Frederiksberg, Denmark.


A wealth of evidence has substantiated GLP-1’s role in regulating appetite and energy intake in humans. Meta-analyses confirm that i.v. infusion of native GLP-1 reduces energy intake in lean and overweight subjects1. A high-protein diet is known to increase satiety and this effect appears to be at least partly mediated by GLP-1. Increased post-prandial GLP-1 levels have been measured in healthy subjects following high-protein meals compared with medium- and low-protein meals, which correlated to increased satiety in the high-protein group2.

Agonists of the GLP-1 receptor, such as exenatide and liraglutide, have been demonstrated to cause weight reduction and decreased food intake in animal models and in patients with type 2 diabetes. Trials are underway to assess efficacy and tolerability in obese patients.

Liraglutide has been shown to cause weight loss in obese patients. Liraglutide 1.2–3.0 mg was compared with placebo or orlistat over 104 weeks in 564 non-diabetic obese individuals3,4. After 52 weeks weight loss was greater with liraglutide 3.0 mg (7.8 kg) vs placebo (2.0 kg) or orlistat (3.9 kg; both P≤0.0001). Nausea and vomiting occurred more often with liraglutide, but adverse events were mainly transient and mild. In another study liraglutide 3.0 mg (n=207) maintained weight lost through diet and exercise for 52 weeks in 81% of subjects compared to 49% of subjects on placebo (n=206; P<0.0001)5. In summary, GLP-1 is an endogenous satiety hormone involved in appetite regulation and GLP-1 receptor agonists are being investigated for the management of obesity.

References: 1. Verdich et al. J Clin Endocrinol Metab 2001 86 4382-9.

2. Belza et al. Obesity Reviews 2011 12 (suppl 1) 59 Oral - T5:0S3.3.

3. Astrup et al. Lancet 2009 374 1606–16.

4. Astrup et al. Int J Obesity 2011. doi: 10.1038/ijo.2011.158.

5. Wadden et al. Diabetes 2011 60 (suppl 1) A502. Poster 1859-P.

Declaration of interest: The author declares that there is a conflict of interest. Details below.

Funding: This work was supported, however funding details are unavailable.

Volume 29

15th International & 14th European Congress of Endocrinology

European Society of Endocrinology 

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