Effect of GLP-1 receptor agonist on gastrointestinal tract motility and residue rates as evaluated by capsule endoscopy - 14/11/17

Doi : 10.1016/j.diabet.2017.05.009

Y. Nakatani ^a,^⁎ , M. Maeda ^b, M. Matsumura ^e, R. Shimizu ^c, N. Banba ^a, Y. Aso ^e, T. Yasu ^c, H. Harasawa ^d
^a Department of Diabetes and Endocrinology, Dokkyo Medical University Nikko Medical Center, 632, Takatoku Nikkoshi, 321-2593 Tochigi, Japan
^b Department of Gastroenterology, Dokkyo Medical University Nikko Medical Center, 632, Takatoku Nikkoshi, 321-2593 Tochigi, Japan
^c Department of Cardiovascular Medicine, Dokkyo Medical University Nikko Medical Center, 632, Takatoku Nikkoshi, 321-2593 Tochigi, Japan
^d Department of Pulmonary Medicine, Dokkyo Medical University Nikko Medical Center, 632, Takatoku Nikkoshi, 321-2593 Tochigi, Japan
^e Department of Endocrinology and Metabolism, Dokkyo Medical University, 880, Kitakobayashi Shimotsugagun Mibumachi, 321-0293 Tochigi, Japan

^⁎Corresponding author.

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Abstract

Aim

This study evaluated the effects of a glucagon-like peptide-1 receptor agonist on gastrointestinal (GI) tract motility and residue rates by examining GI transit time and lumen using capsule endoscopy.

Material and methods

GI motility and lumen were assessed by capsule endoscopy before and after liraglutide administration in 14 patients with type 2 diabetes mellitus (T2DM).

Results

Gastric transit time in the group with diabetic neuropathy (DN) was 1:12:36±1:04:30h before liraglutide administration and 0:48:40±0:32:52h after administration (nonsignificant difference, P=0.19). Gastric transit time in the non-DN group was 1:01:30±0:52:59h before administration and 2:33:29±1:37:24h after administration (significant increase, P=0.03). Duodenal and small intestine transit time in the DN group was 4:10:34±0:25:54h before and 6:38:42±3:52:42h after administration (not significant, P=0.09) and, in the non-DN group, 3:51:03±0:53:47h before and 6:45:31±2:41:36h after administration (significant increase, P=0.03). The GI residue rate in the DN group was 32.1±24% before administration and 90.0±9.1% after administration (significant increase, P<0.001), and increased in all patients; in the non-DN group, it was 32.1±35.3% before and 78.3±23.9% after administration (significant increase, P<0.001), and also increased in all patients.

Conclusion

Liraglutide causes delayed gastric emptying and inhibits duodenal and small intestine motility. However, these GI movement-inhibiting effects may be decreased or absent in patients with DN-associated dysautonomia.

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Keywords : Diabetic neuropathy, Glucagon-like peptide-1, Motility in gastrointestinal tract, Type 2 diabetes mellitus